History of blood types

History of blood types DEFAULT

The Mystery of Human Blood Types

Blood banks run blood type tests before blood is sent to hospitals for transfusions. Image: U.S. Navy photo by Mass Communication Specialist 3rd Class Jake Berenguer/Wikicommons

Everyone’s heard of the A, B, AB and O blood types. When you get a blood transfusion, doctors have to make sure a donor’s blood type is compatible with the recipient’s blood, otherwise the recipient can die. The ABO blood group, as the blood types are collectively known, are ancient. Humans and all other apes share this trait, inheriting these blood types from a common ancestor at least 20 million years ago and maybe even earlier, claims a new study published online today in Proceedings of the National Academy of Sciences. But why humans and apes have these blood types is still a scientific mystery.

The ABO blood group was discovered in the first decade of the 1900s by Austrian physician Karl Landsteiner. Through a series of experiments, Landsteiner classified blood into the four well-known types. The “type” actually refers to the presence of a particular type of antigen sticking up from the surface of a red blood cell. An antigen is anything that elicits a response from an immune cell called an antibody. Antibodies latch onto foreign substances that enter the body, such as bacteria and viruses, and clump them together for removal by other parts of the immune system. The human body naturally makes antibodies that will attack certain types of red-blood-cell antigens. For example, people with type A blood have A antigens on their red blood cells and make antibodies that attack B antigens; people with type B blood have B antigens on their red blood cells and make antibodies that attack A antigens. So, type A people can’t donate their blood to type B people and vice versa. People who are type AB have both A and B antigens on their red blood cells and therefore don’t make any A or B antibodies while people who are type O have no A or B antigens and make both A and B antibodies. (This is hard to keep track of, so I hope the chart below helps!)

After Landsteiner determined the pattern of the ABO blood group, he realized blood types are inherited, and blood typing became one of the first ways to test paternity. Later, researchers learned ABO blood types are governed by  a single gene that comes in three varieties: A, B and O. (People who are type AB inherit an A gene from one parent and a B gene from the other.)

This chart lists the antigens and antibodies made by the different ABO blood types. Image: InvictaHOG/Wikicommons

More than a hundred years after Landsteiner’s Nobel Prize-winning work, scientists still have no idea what function these blood antigens serve. Clearly, people who are type O—the most common blood type—do just fine without them. What scientists have found in the last century, however, are some interesting associations between blood types and disease. In some infectious diseases, bacteria may closely resemble certain blood antigens, making it difficult for antibodies to detect the difference between foreign invaders and the body’s own blood. People who are type A, for instance, seem more susceptible to smallpox, while people who are type B appear more affected by some E. coli infections.

Over the last hundred years, scientists have also discovered that the ABO blood group is just one of more than 20 human blood groups. The Rh factor is another well known blood group, referring to the “positive” or “negative” in blood types, such as A-positive or B-negative. (The Rh refers to Rhesus macaques, which were used in early studies of the blood group.) People who are Rh-positive have Rh antigens on their red blood cells; people who are Rh-negative don’t and produce antibodies that will attack Rh antigens. The Rh blood group plays a role in the sometimes fatal blood disease erythroblastosis fetalis that can develop in newborns if an Rh-negative women gives birth to an Rh-positive baby and her antibodies attack her child.

Most people have never heard of the numerous other blood groups—such as the MN, Diego, Kidd and Kell—probably because they trigger smaller or less frequent immune reactions. And in some cases, like the MN blood group, humans don’t produce antibodies against the antigens. One “minor” blood type that does have medical significance is the Duffy blood group. Plasmodium vivax, one of the parasites that causes malaria, latches onto the Duffy antigen when it invades the body’s red blood cells. People who lack the Duffy antigens, therefore, tend to be immune to this form of malaria.

Although researchers have found these interesting associations between blood groups and disease, they still really don’t understand how and why such blood antigens evolved in the first place. These blood molecules stand as a reminder that we still have a lot to learn about human biology.

Sours: https://www.smithsonianmag.com/science-nature/the-mystery-of-human-blood-types-86993838/

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Distribution of Blood Types

Blood provides an ideal opportunity for the study of human variation without cultural prejudice.  It can be easily classified for many different genetically inherited blood typing systems.  Also significant is the fact that we rarely take blood types into consideration in selecting mates.  In addition, few people know their own type today and no one did prior to 1900.  As a result, differences in blood type frequencies around the world are most likely due to other factors than social discrimination.  Contemporary Japan is somewhat of an exception since there are popular Japanese stereotypes about people with different blood types.  This could affect choice in marriage partners for some Japanese.

All human populations share the same 29 known blood systems, although they differ in the frequencies of specific types.  Given the evolutionary closeness of apes and monkeys to our species, it is not surprising that some of them share a number of blood typing systems with us as well.

When we donate blood or have surgery, a small sample is usually taken in advance for at least ABO click this icon to hear the preceding term pronounced and Rh click this icon to hear the preceding term pronounced systems typing.  If you are O+, the O is your ABO type and the + is your Rh type.  It is possible to be A, B, AB, or O as well as Rh+click this icon to hear the preceding term pronounced or Rh-click this icon to hear the preceding term pronounced.  You inherited your blood types from your parents and the environment in which you live cannot change them.

ABO Blood Type System

We have learned a good deal about how common each of the ABO blood types is around the world.  It is quite clear that the distribution patterns are complex.  Both clinal and discontinuous distributions exist, suggesting a complicated evolutionary history for humanity.  This can be seen with the global frequency patterns of the type B blood allele (shown in the map below).  Note that it is highest in Central Asia and lowest among the indigenous peoples of the Americas and Australia.  However, there are relatively high frequency pockets in Africa as well.  Overall in the world, B is the rarest ABO blood allele.  Only 16% of humanity have it.

map of the world showing the frequency of the B blood allele among indigenous populations--it was absent in Australia, New Zealand, and most of the New World except for western Alaska; it was present throughout the Old World with its highest frequencies in Central and East Asia
Distribution of the B type blood allele in native populations of the world

TheA blood allele is somewhat more common around the world than B.  About 21% of all people share the A allele. The highest frequencies of A are found in small, unrelated populations, especially the Blackfoot Indians of Montana (30-35%), the Australian Aborigines (many groups are 40-53%), and the Lapps, or Saami people, of Northern Scandinavia (50-90%).  The A allele apparently was absent among Central and South American Indians.

map of the world showing the frequency of the A blood allele among indigenous populations--it was absent in Central and South America, but present throughout the rest of the world; it was at its highest frequency in Western Europe, Australia, and the sub-arctic regions of North America and Greenland

Distribution of the A type blood allele in native populations of the world

The O blood type (usually resulting from the absence of both A and B alleles) is very common around the world.  About 63% of humans share it.  Type Ois particularly high in frequency among the indigenous populations of Central and South America, where it approaches 100%.  It also is relatively high among Australian Aborigines and in Western Europe (especially in populations with Celtic ancestors).  The lowest frequency of O is found in Eastern Europe and Central Asia, where B is common.

map of the world showing the frequency of the O blood allele among indigenous populations--most regions were 50% or higher in frequency; it was highest in the New World (90-100%) and lowest in Central Asia (50-60%)
Distribution of the O type blood in native populations of the world

Other Blood Type Systems

The majority of the people in the world have the Rh+ blood type.  However, it is more common in some regions.  Native Americans and Australian Aborigines were very likely 99-100% Rh+ before they began interbreeding with people from other parts of the world.  This does not imply that Native Americans and Australian Aborigines are historically closely related to each other.  Most Subsaharan African populations are around 97-99% Rh+.  East Asians are 93-99+% Rh+.  Europeans have the lowest frequency of this blood type for any continent.  They are 83-85% Rh+.  The lowest known frequency is found among the Basques of the Pyrenees Mountains between France and Spain.  They are only 65% Rh+.

The distribution patterns for the Diegoclick this icon to hear the preceding term pronounced blood system are even more striking.  Evidently, all Africans, Europeans, East Indians, Australian Aborigines, and Polynesians are Diego negative.  The only populations with Diego positive people may be Native Americans (2-46%) and East Asians (3-12%).  This nonrandom distribution pattern fits well with the hypothesis of an East Asian origin for Native Americans.


These patterns of ABO, Rh, and Diego blood type distributions are not similar to those for skin color or other so-called "racial" traits.  The implication is that the specific causes responsible for the distribution of human blood types have been different than those for other traits that have been commonly employed to categorize people into "races."  Since it would be possible to divide up humanity into radically different groupings using blood typing instead of other genetically inherited traits such as skin color, we have more conclusive evidence that the commonly used typological model for understanding human variation is scientifically unsound.

The more we study the precise details of human variation, the more we understand how complex are the patterns.  They cannot be easily summarized or understood.  Yet, this hard-earned scientific knowledge is generally ignored in most countries because of more demanding social and political concerns.  As a result, discrimination based on presumed "racial" groups still continues.  It is important to keep in mind that this "racial" classification often has more to do with cultural and historical distinctions than it does with biology.  In a very real sense, "race" is a distinction that is created by culture not biology.


Copyright � 1998-2012 by Dennis O'Neil. All rights reserved.
illustration credits

Sours: https://www2.palomar.edu/anthro/vary/vary_3.htm

Why do we have blood types?

More than a century after their discovery, we still don’t really know what blood types are for. Do they really matter? Carl Zimmer investigates.

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When my parents informed me that my blood type was A+, I felt a strange sense of pride. If A+ was the top grade in school, then surely A+ was also the most excellent of blood types – a biological mark of distinction.

It didn’t take long for me to recognise just how silly that feeling was and tamp it down. But I didn’t learn much more about what it really meant to have type A+ blood. By the time I was an adult, all I really knew was that if I should end up in a hospital in need of blood, the doctors there would need to make sure they transfused me with a suitable type.

And yet there remained some nagging questions. Why do 40 per cent of Caucasians have type A blood, while only 27 per cent of Asians do? Where do different blood types come from, and what do they do? To get some answers, I went to the experts – to haematologists, geneticists, evolutionary biologists, virologists and nutrition scientists.

In 1900 the Austrian physician Karl Landsteiner first discovered blood types, winning the Nobel Prize in Physiology or Medicine for his research in 1930. Since then scientists have developed ever more powerful tools for probing the biology of blood types. They’ve found some intriguing clues about them – tracing their deep ancestry, for example, and detecting influences of blood types on our health. And yet I found that in many ways blood types remain strangely mysterious. Scientists have yet to come up with a good explanation for their very existence.

“Isn’t it amazing?” says Ajit Varki, a biologist at the University of California, San Diego. “Almost a hundred years after the Nobel Prize was awarded for this discovery, we still don’t know exactly what they’re for.”

My knowledge that I’m type A comes to me thanks to one of the greatest discoveries in the history of medicine. Because doctors are aware of blood types, they can save lives by transfusing blood into patients. But for most of history, the notion of putting blood from one person into another was a feverish dream.

Renaissance doctors mused about what would happen if they put blood into the veins of their patients. Some thought that it could be a treatment for all manner of ailments, even insanity. Finally, in the 1600s, a few doctors tested out the idea, with disastrous results. A French doctor injected calf’s blood into a madman, who promptly started to sweat and vomit and produce urine the colour of chimney soot. After another transfusion the man died.

Such calamities gave transfusions a bad reputation for 150 years. Even in the 19th century only a few doctors dared try out the procedure. One of them was a British physician named James Blundell. Like other physicians of his day, he watched many of his female patients die from bleeding during childbirth. After the death of one patient in 1817, he found he couldn’t resign himself to the way things were.

“I could not forbear considering, that the patient might very probably have been saved by transfusion,” he later wrote.

Human patients should only get human blood, Blundell decided. But no one had ever tried to perform such a transfusion. Blundell set about doing so by designing a system of funnels and syringes and tubes that could channel blood from a donor to an ailing patient. After testing the apparatus out on dogs, Blundell was summoned to the bed of a man who was bleeding to death. “Transfusion alone could give him a chance of life,” he wrote.

Several donors provided Blundell with 14 ounces of blood, which he injected into the man’s arm. After the procedure the patient told Blundell that he felt better – “less fainty” – but two days later he died.

Still, the experience convinced Blundell that blood transfusion would be a huge benefit to mankind, and he continued to pour blood into desperate patients in the following years. All told, he performed ten blood transfusions. Only four patients survived.

While some other doctors experimented with blood transfusion as well, their success rates were also dismal. Various approaches were tried, including attempts in the 1870s to use milk in transfusions (which were, unsurprisingly, fruitless and dangerous).

Blundell was correct in believing that humans should only get human blood. But he didn’t know another crucial fact about blood: that humans should only get blood from certain other humans. It’s likely that Blundell’s ignorance of this simple fact led to the death of some of his patients. What makes those deaths all the more tragic is that the discovery of blood types, a few decades later, was the result of a fairly simple procedure.

The first clues as to why the transfusions of the early 19th century had failed were clumps of blood. When scientists in the late 1800s mixed blood from different people in test tubes, they noticed that sometimes the red blood cells stuck together. But because the blood generally came from sick patients, scientists dismissed the clumping as some sort of pathology not worth investigating. Nobody bothered to see if the blood of healthy people clumped, until Karl Landsteiner wondered what would happen. Immediately, he could see that mixtures of healthy blood sometimes clumped too.

Landsteiner set out to map the clumping pattern, collecting blood from members of his lab, including himself. He separated each sample into red blood cells and plasma, and then he combined plasma from one person with cells from another.

Landsteiner found that the clumping occurred only if he mixed certain people’s blood together. By working through all the combinations, he sorted his subjects into three groups. He gave them the entirely arbitrary names of A, B and C. (Later on C was renamed O, and a few years later other researchers discovered the AB group. By the middle of the 20th century the American researcher Philip Levine had discovered another way to categorise blood, based on whether it had the Rh blood factor. A plus or minus sign at the end of Landsteiner’s letters indicates whether a person has the factor or not.)

When Landsteiner mixed the blood from different people together, he discovered it followed certain rules. If he mixed the plasma from group A with red blood cells from someone else in group A, the plasma and cells remained a liquid. The same rule applied to the plasma and red blood cells from group B. But if Landsteiner mixed plasma from group A with red blood cells from B, the cells clumped (and vice versa).

The blood from people in group O was different. When Landsteiner mixed either A or B red blood cells with O plasma, the cells clumped. But he could add A or B plasma to O red blood cells without any clumping.

It’s this clumping that makes blood transfusions so potentially dangerous. If a doctor accidentally injected type B blood into my arm, my body would become loaded with tiny clots. They would disrupt my circulation and cause me to start bleeding massively, struggle for breath and potentially die. But if I received either type A or type O blood, I would be fine.

Landsteiner didn’t know what precisely distinguished one blood type from another. Later generations of scientists discovered that the red blood cells in each type are decorated with different molecules on their surface. In my type A blood, for example, the cells build these molecules in two stages, like two floors of a house. The first floor is called an H antigen. On top of the first floor the cells build a second, called the A antigen.

People with type B blood, on the other hand, build the second floor of the house in a different shape. And people with type O build a single-storey ranch house: they only build the H antigen and go no further.

Each person’s immune system becomes familiar with his or her own blood type. If people receive a transfusion of the wrong type of blood, however, their immune system responds with a furious attack, as if the blood were an invader. The exception to this rule is type O blood. It only has H antigens, which are present in the other blood types too. To a person with type A or type B, it seems familiar. That familiarity makes people with type O blood universal donors, and their blood especially valuable to blood centres.

Landsteiner reported his experiment in a short, terse paper in 1900. “It might be mentioned that the reported observations may assist in the explanation of various consequences of therapeutic blood transfusions,” he concluded with exquisite understatement. Landsteiner’s discovery opened the way to safe, large-scale blood transfusions, and even today blood banks use his basic method of clumping blood cells as a quick, reliable test for blood types.

But as Landsteiner answered an old question, he raised new ones. What, if anything, were blood types for? Why should red blood cells bother with building their molecular houses? And why do people have different houses?

Solid scientific answers to these questions have been hard to come by. And in the meantime, some unscientific explanations have gained huge popularity. “It’s just been ridiculous,” sighs Connie Westhoff, the Director of Immunohematology, Genomics, and Rare Blood at the New York Blood Center. 

In 1996 a naturopath named Peter D’Adamo published a book called Eat Right 4 Your Type. D’Adamo argued that we must eat according to our blood type, in order to harmonise with our evolutionary heritage.

Blood types, he claimed, “appear to have arrived at critical junctures of human development.” According to D’Adamo, type O blood arose in our hunter-gatherer ancestors in Africa, type A at the dawn of agriculture, and type B developed between 10,000 and 15,000 years ago in the Himalayan highlands. Type AB, he argued, is a modern blending of A and B.

From these suppositions D’Adamo then claimed that our blood type determines what food we should eat. With my agriculture-based type A blood, for example, I should be a vegetarian. People with the ancient hunter type O should have a meat-rich diet and avoid grains and dairy. According to the book, foods that aren’t suited to our blood type contain antigens that can cause all sorts of illness. D’Adamo recommended his diet as a way to reduce infections, lose weight, fight cancer and diabetes, and slow the ageing process.

D’Adamo’s book has sold 7 million copies and has been translated into 60 languages. It’s been followed by a string of other blood type diet books; D’Adamo also sells a line of blood-type-tailored diet supplements on his website. As a result, doctors often get asked by their patients if blood type diets actually work.

The best way to answer that question is to run an experiment. In Eat Right 4 Your Type D’Adamo wrote that he was in the eighth year of a decade-long trial of blood type diets on women with cancer. Eighteen years later, however, the data from this trial have not yet been published.

Recently, researchers at the Red Cross in Belgium decided to see if there was any other evidence in the diet’s favour. They hunted through the scientific literature for experiments that measured the benefits of diets based on blood types. Although they examined over 1,000 studies, their efforts were futile. “There is no direct evidence supporting the health effects of the ABO blood type diet,” says Emmy De Buck of the Belgian Red Cross-Flanders.

After De Buck and her colleagues published their review in the American Journal of Clinical Nutrition, D’Adamo responded on his blog. In spite of the lack of published evidence supporting his Blood Type Diet, he claimed that the science behind it is right. “There is good science behind the blood type diets, just like there was good science behind Einstein’s mathmatical [sic] calculations that led to the Theory of Relativity,” he wrote.

Comparisons to Einstein notwithstanding, the scientists who actually do research on blood types categorically reject such a claim. “The promotion of these diets is wrong,” a group of researchers flatly declared in Transfusion Medicine Reviews.

Nevertheless, some people who follow the Blood Type Diet see positive results. According to Ahmed El-Sohemy, a nutritional scientist at the University of Toronto, that’s no reason to think that blood types have anything to do with the diet’s success.

El-Sohemy is an expert in the emerging field of nutrigenomics. He and his colleagues have brought together 1,500 volunteers to study, tracking the foods they eat and their health. They are analysing the DNA of their subjects to see how their genes may influence how food affects them. Two people may respond very differently to the same diet based on their genes.

“Almost every time I give talks about this, someone at the end asks me, ‘Oh, is this like the Blood Type Diet?’” says El-Sohemy. As a scientist, he found Eat Right 4 Your Type lacking. “None of the stuff in the book is backed by science,” he says. But El-Sohemy realised that since he knew the blood types of his 1,500 volunteers, he could see if the Blood Type Diet actually did people any good.

El-Sohemy and his colleagues divided up their subjects by their diets. Some ate the meat-based diets D’Adamo recommended for type O, some ate a mostly vegetarian diet as recommended for type A, and so on. The scientists gave each person in the study a score for how well they adhered to each blood type diet.

The researchers did find, in fact, that some of the diets could do people some good. People who stuck to the type A diet, for example, had lower body mass index scores, smaller waists and lower blood pressure. People on the type O diet had lower triglycerides. The type B diet – rich in dairy products – provided no benefits.

“The catch,” says El-Sohemy, “is that it has nothing to do with people’s blood type.” In other words, if you have type O blood, you can still benefit from a so-called type A diet just as much as someone with type A blood – probably because the benefits of a mostly vegetarian diet can be enjoyed by anyone. Anyone on a type O diet cuts out lots of carbohydrates, with the attending benefits of this being available to virtually everyone. Likewise, a diet rich in dairy products isn’t healthy for anyone – no matter their blood type.

One of the appeals of the Blood Type Diet is its story of the origins of how we got our different blood types. But that story bears little resemblance to the evidence that scientists have gathered about their evolution.

After Landsteiner’s discovery of human blood types in 1900, other scientists wondered if the blood of other animals came in different types too. It turned out that some primate species had blood that mixed nicely with certain human blood types. But for a long time it was hard to know what to make of the findings. The fact that a monkey’s blood doesn’t clump with my type A blood doesn’t necessarily mean that the monkey inherited the same type A gene that I carry from a common ancestor we share. Type A blood might have evolved more than once.

The uncertainty slowly began to dissolve, starting in the 1990s with scientists deciphering the molecular biology of blood types. They found that a single gene, called ABO, is responsible for building the second floor of the blood type house. The A version of the gene differs by a few key mutations from B. People with type O blood have mutations in the ABO gene that prevent them from making the enzyme that builds either the A or B antigen.

Scientists could then begin comparing the ABO gene from humans to other species. Laure Ségurel and her colleagues at the National Center for Scientific Research in Paris have led the most ambitious survey of ABO genes in primates to date. And they’ve found that our blood types are profoundly old. Gibbons and humans both have variants for both A and B blood types, and those variants come from a common ancestor that lived 20 million years ago.

Our blood types might be even older, but it’s hard to know how old. Scientists have yet to analyse the genes of all primates, so they can’t see how widespread our own versions are among other species. But the evidence that scientists have gathered so far already reveals a turbulent history to blood types. In some lineages mutations have shut down one blood type or another. Chimpanzees, our closest living relatives, have only type A and type O blood. Gorillas, on the other hand, have only B. In some cases mutations have altered the ABO gene, turning type A blood into type B. And even in humans, scientists are finding, mutations have repeatedly arisen that prevent the ABO protein from building a second storey on the blood type house. These mutations have turned blood types from A or B to O. “There are hundreds of ways of being type O,” says Westhoff.

Being type A is not a legacy of my proto-farmer ancestors, in other words. It’s a legacy of my monkey-like ancestors. Surely, if my blood type has endured for millions of years, it must be providing me with some obvious biological benefit. Otherwise, why do my blood cells bother building such complicated molecular structures?

Yet scientists have struggled to identify what benefit the ABO gene provides. “There is no good and definite explanation for ABO,” says Antoine Blancher of the University of Toulouse, “although many answers have been given.”

The most striking demonstration of our ignorance about the benefit of blood types came to light in Bombay in 1952. Doctors discovered that a handful of patients had no ABO blood type at all – not A, not B, not AB, not O. If A and B are two-storey buildings, and O is a one-storey ranch house, then these Bombay patients had only an empty lot.

Since its discovery this condition – called the Bombay phenotype – has turned up in other people, although it remains exceedingly rare. And as far as scientists can tell, there’s no harm that comes from it. The only known medical risk it presents comes when it’s time for a blood transfusion. Those with the Bombay phenotype can only accept blood from other people with the same condition. Even blood type O, supposedly the universal blood type, can kill them.

The Bombay phenotype proves that there’s no immediate life-or-death advantage to having ABO blood types. Some scientists think that the explanation for blood types may lie in their variation. That’s because different blood types may protect us from different diseases.

Doctors first began to notice a link between blood types and different diseases in the middle of the 20th century, and the list has continued to grow. “There are still many associations being found between blood groups and infections, cancers and a range of diseases,” Pamela Greenwell of the University of Westminster tells me.

From Greenwell I learn to my displeasure that blood type A puts me at a higher risk of several types of cancer, such as some forms of pancreatic cancer and leukaemia. I’m also more prone to smallpox infections, heart disease and severe malaria. On the other hand, people with other blood types have to face increased risks of other disorders. People with type O, for example, are more likely to get ulcers and ruptured Achilles tendons.

These links between blood types and diseases have a mysterious arbitrariness about them, and scientists have only begun to work out the reasons behind some of them. For example, Kevin Kain of the University of Toronto and his colleagues have been investigating why people with type O are better protected against severe malaria than people with other blood types. His studies indicate that immune cells have an easier job of recognising infected blood cells if they’re type O rather than other blood types.

More puzzling are the links between blood types and diseases that have nothing to do with the blood. Take norovirus. This nasty pathogen is the bane of cruise ships, as it can rage through hundreds of passengers, causing violent vomiting and diarrhoea. It does so by invading cells lining the intestines, leaving blood cells untouched. Nevertheless, people’s blood type influences the risk that they will be infected by a particular strain of norovirus.

The solution to this particular mystery can be found in the fact that blood cells are not the only cells to produce blood type antigens. They are also produced by cells in blood vessel walls, the airway, skin and hair. Many people even secrete blood type antigens in their saliva. Noroviruses make us sick by grabbing onto the blood type antigens produced by cells in the gut.

Yet a norovirus can only grab firmly onto a cell if its proteins fit snugly onto the cell’s blood type antigen. So it’s possible that each strain of norovirus has proteins that are adapted to attach tightly to certain blood type antigens, but not others. That would explain why our blood type can influence which norovirus strains can make us sick.

It may also be a clue as to why a variety of blood types have endured for millions of years. Our primate ancestors were locked in a never-ending cage match with countless pathogens, including viruses, bacteria and other enemies. Some of those pathogens may have adapted to exploit different kinds of blood type antigens. The pathogens that were best suited to the most common blood type would have fared best, because they had the most hosts to infect. But, gradually, they may have destroyed that advantage by killing off their hosts. Meanwhile, primates with rarer blood types would have thrived, thanks to their protection against some of their enemies.

As I contemplate this possibility, my type A blood remains as puzzling to me as when I was a boy. But it’s a deeper state of puzzlement that brings me some pleasure. I realise that the reason for my blood type may, ultimately, have nothing to do with blood at all.


A biography of Karl Landsteiner.

Landsteiner’s report on his blood clumping experiments, first published in 1900.

A biography of James Blundell.

A history of blood transfusion detailing the work of Blundell.

Blundell’s ownaccounts of his transfusion experiments.

Eat Right 4 Your Type, Peter D’Adamo’s diet book first published in 1996.

Emmy De Buck and her colleagues’ article on the lack of supporting evidence for blood type diets, published in the American Journal of Clinical Nutrition in 2013.

The 2012 article in Transfusion Medicine Reviews that argues against promoting blood type diets.

Ahmed El-Sohemy and colleagues’ 2014 paper that tests the validity of blood type diets.

Laure Ségurel and colleagues’ 2013 paper on the evolutionary history of the ABO blood groups.

Sours: https://mosaicscience.com/story/why-do-we-have-blood-types

Of blood types history

Blood type

Classification of blood

This article is about blood type in humans. For other uses, see Blood type (disambiguation).

Blood type (or blood group) is determined, in part, by the ABO blood group antigens present on red blood cells.

A blood type (also known as a blood group) is a classification of blood, based on the presence and absence of antibodies and inheritedantigenic substances on the surface of red blood cells (RBCs). These antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood group system. Some of these antigens are also present on the surface of other types of cells of various tissues. Several of these red blood cell surface antigens can stem from one allele (or an alternative version of a gene) and collectively form a blood group system.[1]

Blood types are inherited and represent contributions from both parents. As of 2019[update], a total of 41 human blood group systems are recognized by the International Society of Blood Transfusion (ISBT).[2] The two most important blood group systems are ABO and Rh; they determine someone's blood type (A, B, AB, and O, with +, − or null denoting RhD status) for suitability in blood transfusion.

Blood group systems[edit]

Main article: Human blood group systems

A complete blood type would describe each of the 38 blood groups, and an individual's blood type is one of many possible combinations of blood-group antigens.[2] Almost always, an individual has the same blood group for life, but very rarely an individual's blood type changes through addition or suppression of an antigen in infection, malignancy, or autoimmune disease.[3][4][5][6] Another more common cause of blood type change is a bone marrow transplant. Bone-marrow transplants are performed for many leukemias and lymphomas, among other diseases. If a person receives bone marrow from someone who is a different ABO type (e.g., a type A patient receives a type O bone marrow), the patient's blood type will eventually convert to the donor's type.

Some blood types are associated with inheritance of other diseases; for example, the Kell antigen is sometimes associated with McLeod syndrome.[7] Certain blood types may affect susceptibility to infections, an example being the resistance to specific malaria species seen in individuals lacking the Duffy antigen.[8] The Duffy antigen, presumably as a result of natural selection, is less common in population groups from areas having a high incidence of malaria.[9]

ABO blood group system[edit]

ABO blood group system: diagram showing the carbohydrate chains that determine the ABO blood group

Main article: ABO blood group system

The ABO blood group system involves two antigens and two antibodies found in human blood. The two antigens are antigen A and antigen B. The two antibodies are antibody A and antibody B. The antigens are present on the red blood cells and the antibodies in the serum. Regarding the antigen property of the blood all human beings can be classified into 4 groups, those with antigen A (group A), those with antigen B (group B), those with both antigen A and B (group AB) and those with neither antigen (group O). The antibodies present together with the antigens are found as follows:

  1. Antigen A with antibody B
  2. Antigen B with antibody A
  3. Antigen AB has no antibodies
  4. Antigen nil (group O) with antibody A and B.

There is an agglutination reaction between similar antigen and antibody (for example, antigen A agglutinates the antibody A and antigen B agglutinates the antibody B). Thus, transfusion can be considered safe as long as the serum of the recipient does not contain antibodies for the blood cell antigens of the donor.

The ABO system is the most important blood-group system in human-blood transfusion. The associated anti-A and anti-B antibodies are usually immunoglobulin M, abbreviated IgM, antibodies. It has been hypothesized that ABO IgM antibodies are produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses, although blood group compatibility rules are applied to newborn and infants as a matter of practice.[10] The original terminology used by Karl Landsteiner in 1901 for the classification was A/B/C; in later publications "C" became "O".[11] Type O is often called 0 (zero, or null) in other languages.[11][12]

Rh blood group system[edit]

Main article: Rh blood group system

The Rh system (Rh meaning Rhesus) is the second most significant blood-group system in human-blood transfusion with currently 50 antigens. The most significant Rh antigen is the D antigen, because it is the most likely to provoke an immune system response of the five main Rh antigens. It is common for D-negative individuals not to have any anti-D IgG or IgM antibodies, because anti-D antibodies are not usually produced by sensitization against environmental substances. However, D-negative individuals can produce IgG anti-D antibodies following a sensitizing event: possibly a fetomaternal transfusion of blood from a fetus in pregnancy or occasionally a blood transfusion with D positive RBCs.[13]Rh disease can develop in these cases.[14] Rh negative blood types are much less common in Asian populations (0.3%) than they are in European populations (15%).[15] The presence or absence of the Rh(D) antigen is signified by the + or − sign, so that, for example, the A− group is ABO type A and does not have the Rh (D) antigen.

ABO and Rh distribution by country[edit]

Main article: Blood type distribution by country

As with many other genetic traits, the distribution of ABO and Rh blood groups varies significantly between populations.

Other blood group systems[edit]

Main article: Human blood group systems

As of 2019[update], 36 blood-group systems have been identified by the International Society for Blood Transfusion in addition to the ABO and Rh systems.[2] Thus, in addition to the ABO antigens and Rh antigens, many other antigens are expressed on the RBC surface membrane. For example, an individual can be AB, D positive, and at the same time M and N positive (MNS system), K positive (Kell system), Lea or Leb negative (Lewis system), and so on, being positive or negative for each blood group system antigen. Many of the blood group systems were named after the patients in whom the corresponding antibodies were initially encountered. Blood group systems other than ABO and Rh pose a potential, yet relatively low, risk of complications upon mixing of blood from different people.[16]

Following is a comparison of clinically relevant characteristics of antibodies against the main human blood group systems:[17]

Naturally occurring YesNoNoNoNo
Most common in immediate hemolytic transfusion reactions AYesFyaJka
Most common in delayed hemolytic transfusion reactions E,D,CJka
Most common in hemolytic disease of the newbornYesD,CYes
Commonly produce intravascular hemolysis YesYes

Clinical significance[edit]

Blood transfusion[edit]

Main article: Blood transfusion

Transfusion medicine is a specialized branch of hematology that is concerned with the study of blood groups, along with the work of a blood bank to provide a transfusion service for blood and other blood products. Across the world, blood products must be prescribed by a medical doctor (licensed physician or surgeon) in a similar way as medicines.

Much of the routine work of a blood bank involves testing blood from both donors and recipients to ensure that every individual recipient is given blood that is compatible and is as safe as possible. If a unit of incompatible blood is transfused between a donor and recipient, a severe acute hemolytic reaction with hemolysis (RBC destruction), kidney failure and shock is likely to occur, and death is a possibility. Antibodies can be highly active and can attack RBCs and bind components of the complement system to cause massive hemolysis of the transfused blood.

Patients should ideally receive their own blood or type-specific blood products to minimize the chance of a transfusion reaction. It is also possible to use the patient's own blood for transfusion. This is called autologous blood transfusion, which is always compatible with the patient. The procedure of washing a patient's own red blood cells goes as follows: The patient's lost blood is collected and washed with a saline solution. The washing procedure yields concentrated washed red blood cells. The last step is reinfusing the packed red blood cells into the patient. There are multiple ways to wash red blood cells. The two main ways are centrifugation and filtration methods. This procedure can be performed with microfiltration devices like the Hemoclear filter. Risks can be further reduced by cross-matching blood, but this may be skipped when blood is required for an emergency. Cross-matching involves mixing a sample of the recipient's serum with a sample of the donor's red blood cells and checking if the mixture agglutinates, or forms clumps. If agglutination is not obvious by direct vision, blood bank technicians usually check for agglutination with a microscope. If agglutination occurs, that particular donor's blood cannot be transfused to that particular recipient. In a blood bank it is vital that all blood specimens are correctly identified, so labelling has been standardized using a barcode system known as ISBT 128.

The blood group may be included on identification tags or on tattoos worn by military personnel, in case they should need an emergency blood transfusion. Frontline German Waffen-SS had blood group tattoos during World War II.

Rare blood types can cause supply problems for blood banks and hospitals. For example, Duffy-negative blood occurs much more frequently in people of African origin,[20] and the rarity of this blood type in the rest of the population can result in a shortage of Duffy-negative blood for these patients. Similarly, for RhD negative people there is a risk associated with travelling to parts of the world where supplies of RhD negative blood are rare, particularly East Asia, where blood services may endeavor to encourage Westerners to donate blood.[21]

Hemolytic disease of the newborn (HDN)[edit]

Main article: Hemolytic disease of the newborn

A pregnant woman may carry a fetus with a blood type which is different from her own. Typically, this is an issue if a Rh- mother has a child with a Rh+ father, and the fetus ends up being Rh+ like the father.[22] In those cases, the mother can make IgG blood group antibodies. This can happen if some of the fetus' blood cells pass into the mother's blood circulation (e.g. a small fetomaternal hemorrhage at the time of childbirth or obstetric intervention), or sometimes after a therapeutic blood transfusion. This can cause Rh disease or other forms of hemolytic disease of the newborn (HDN) in the current pregnancy and/or subsequent pregnancies. Sometimes this is lethal for the fetus; in these cases it is called hydrops fetalis.[23] If a pregnant woman is known to have anti-D antibodies, the Rh blood type of a fetus can be tested by analysis of fetal DNA in maternal plasma to assess the risk to the fetus of Rh disease.[24] One of the major advances of twentieth century medicine was to prevent this disease by stopping the formation of Anti-D antibodies by D negative mothers with an injectable medication called Rho(D) immune globulin.[25][26] Antibodies associated with some blood groups can cause severe HDN, others can only cause mild HDN and others are not known to cause HDN.[23]

Blood products[edit]

To provide maximum benefit from each blood donation and to extend shelf-life, blood banksfractionate some whole blood into several products. The most common of these products are packed RBCs, plasma, platelets, cryoprecipitate, and fresh frozen plasma (FFP). FFP is quick-frozen to retain the labile clotting factorsV and VIII, which are usually administered to patients who have a potentially fatal clotting problem caused by a condition such as advanced liver disease, overdose of anticoagulant, or disseminated intravascular coagulation (DIC).

Units of packed red cells are made by removing as much of the plasma as possible from whole blood units.

Clotting factors synthesized by modern recombinant methods are now in routine clinical use for hemophilia, as the risks of infection transmission that occur with pooled blood products are avoided.

Red blood cell compatibility[edit]

Further information: Blood compatibility testing

  • Blood group AB individuals have both A and B antigens on the surface of their RBCs, and their blood plasma does not contain any antibodies against either A or B antigen. Therefore, an individual with type AB blood can receive blood from any group (with AB being preferable), but cannot donate blood to any group other than AB. They are known as universal recipients.
  • Blood group A individuals have the A antigen on the surface of their RBCs, and blood serum containing IgM antibodies against the B antigen. Therefore, a group A individual can receive blood only from individuals of groups A or O (with A being preferable), and can donate blood to individuals with type A or AB.
  • Blood group B individuals have the B antigen on the surface of their RBCs, and blood serum containing IgM antibodies against the A antigen. Therefore, a group B individual can receive blood only from individuals of groups B or O (with B being preferable), and can donate blood to individuals with type B or AB.
  • Blood group O (or blood group zero in some countries) individuals do not have either A or B antigens on the surface of their RBCs, and their blood serum contains IgM anti-A and anti-B antibodies. Therefore, a group O individual can receive blood only from a group O individual, but can donate blood to individuals of any ABO blood group (i.e., A, B, O or AB). If a patient needs an urgent blood transfusion, and if the time taken to process the recipient's blood would cause a detrimental delay, O negative blood can be issued. Because it is compatible with anyone, O negative blood is often overused and consequently is always in short supply.[27] According to the American Association of Blood Banks and the British Chief Medical Officer's National Blood Transfusion Committee, the use of group O RhD negative red cells should be restricted to persons with O negative blood, women who might be pregnant, and emergency cases in which blood-group testing is genuinely impracticable.[27]
Red blood cell compatibility chart
In addition to donating to the same blood group; type O blood donors can give to A, B and AB; blood donors of types A and B can give to AB.

Table note
1. Assumes absence of atypical antibodies that would cause an incompatibility between donor and recipient blood, as is usual for blood selected by cross matching.

An Rh D-negative patient who does not have any anti-D antibodies (never being previously sensitized to D-positive RBCs) can receive a transfusion of D-positive blood once, but this would cause sensitization to the D antigen, and a female patient would become at risk for hemolytic disease of the newborn. If a D-negative patient has developed anti-D antibodies, a subsequent exposure to D-positive blood would lead to a potentially dangerous transfusion reaction. Rh D-positive blood should never be given to D-negative women of child-bearing age or to patients with D antibodies, so blood banks must conserve Rh-negative blood for these patients. In extreme circumstances, such as for a major bleed when stocks of D-negative blood units are very low at the blood bank, D-positive blood might be given to D-negative females above child-bearing age or to Rh-negative males, providing that they did not have anti-D antibodies, to conserve D-negative blood stock in the blood bank. The converse is not true; Rh D-positive patients do not react to D negative blood.

This same matching is done for other antigens of the Rh system as C, c, E and e and for other blood group systems with a known risk for immunization such as the Kell system in particular for females of child-bearing age or patients with known need for many transfusions.

Plasma compatibility[edit]

Plasma compatibility chart
In addition to donating to the same blood group; plasma from type AB can be given to A, B and O; plasma from types A, B and AB can be given to O.

Blood plasma compatibility is the inverse of red blood cell compatibility.[30] Type AB plasma carries neither anti-A nor anti-B antibodies and can be transfused to individuals of any blood group; but type AB patients can only receive type AB plasma. Type O carries both antibodies, so individuals of blood group O can receive plasma from any blood group, but type O plasma can be used only by type O recipients.

Table note
1. Assumes absence of strong atypical antibodies in donor plasma

Rh D antibodies are uncommon, so generally neither D negative nor D positive blood contain anti-D antibodies. If a potential donor is found to have anti-D antibodies or any strong atypical blood group antibody by antibody screening in the blood bank, they would not be accepted as a donor (or in some blood banks the blood would be drawn but the product would need to be appropriately labeled); therefore, donor blood plasma issued by a blood bank can be selected to be free of D antibodies and free of other atypical antibodies, and such donor plasma issued from a blood bank would be suitable for a recipient who may be D positive or D negative, as long as blood plasma and the recipient are ABO compatible.[citation needed]

Universal donors and universal recipients[edit]

A hospital worker takes samples of blood from a donor for testing

In transfusions of packed red blood cells, individuals with type O Rh D negative blood are often called universal donors. Those with type AB Rh D positive blood are called universal recipients. However, these terms are only generally true with respect to possible reactions of the recipient's anti-A and anti-B antibodies to transfused red blood cells, and also possible sensitization to Rh D antigens. One exception is individuals with hh antigen system (also known as the Bombay phenotype) who can only receive blood safely from other hh donors, because they form antibodies against the H antigen present on all red blood cells.[32][33]

Blood donors with exceptionally strong anti-A, anti-B or any atypical blood group antibody may be excluded from blood donation. In general, while the plasma fraction of a blood transfusion may carry donor antibodies not found in the recipient, a significant reaction is unlikely because of dilution.

Additionally, red blood cell surface antigens other than A, B and Rh D, might cause adverse reactions and sensitization, if they can bind to the corresponding antibodies to generate an immune response. Transfusions are further complicated because platelets and white blood cells (WBCs) have their own systems of surface antigens, and sensitization to platelet or WBC antigens can occur as a result of transfusion.

For transfusions of plasma, this situation is reversed. Type O plasma, containing both anti-A and anti-B antibodies, can only be given to O recipients. The antibodies will attack the antigens on any other blood type. Conversely, AB plasma can be given to patients of any ABO blood group, because it does not contain any anti-A or anti-B antibodies.

Blood typing[edit]

Main article: Blood typing

Typically, blood type tests are performed through addition of a blood sample to a solution containing antibodies corresponding to each antigen. The presence of an antigen on the surface of the blood cells is indicated by agglutination. In these tests, rather than agglutination, a positive result is indicated by decolorization as red blood cells which bind to the nanoparticles are pulled toward a magnet and removed from solution.

Blood group genotyping[edit]

In addition to the current practice of serologic testing of blood types, the progress in molecular diagnostics allows the increasing use of blood group genotyping. In contrast to serologic tests reporting a direct blood type phenotype, genotyping allows the prediction of a phenotype based on the knowledge of the molecular basis of the currently known antigens. This allows a more detailed determination of the blood type and therefore a better match for transfusion, which can be crucial in particular for patients with needs for many transfusions to prevent allo-immunization.[34][35]


Blood types were first discovered by an Austrian physician, Karl Landsteiner, working at the Pathological-Anatomical Institute of the University of Vienna (now Medical University of Vienna). In 1900, he found that blood sera from different persons would clump together (agglutinate) when mixed in test tubes, and not only that, some human blood also agglutinated with animal blood.[36] He wrote a two-sentence footnote:

The serum of healthy human beings not only agglutinates animal red cells, but also often those of human origin, from other individuals. It remains to be seen whether this appearance is related to inborn differences between individuals or it is the result of some damage of bacterial kind.[37]

This was the first evidence that blood variation exists in humans. The next year, in 1901, he made a definitive observation that blood serum of an individual would agglutinate with only those of certain individuals. Based on this he classified human bloods into three groups, namely group A, group B, and group C. He defined that group A blood agglutinates with group B, but never with its own type. Similarly, group B blood agglutinates with group A. Group C blood is different in that it agglutinates with both A and B.[38] This was the discovery of blood groups for which Landsteiner was awarded the Nobel Prize in Physiology or Medicine in 1930. (C was later renamed to O after the German Ohne, meaning without, or zero, or null.[39]) Another group (later named AB) was discovered a year later by Landsteiner's students Adriano Sturli and Alfred von Decastello without designating the name (simply referring it to as "no particular type").[40][41] Thus, after Landsteiner, three blood types were initially recognised, namely A, B, and C.[41]

Czech serologist Jan Janský was the first to recognise and designate four blood types in 1907 that he published in a local journal,[42] using the Roman numerical I, II, III, and IV (corresponding to modern O, A, B, and AB respectively).[43] Unknown to Janský, an American physician William L. Moss introduced almost identical classification in 1910;[44] but his I and IV corresponding Janský's IV and I.[45] Moss came across Janský's paper as his was being printed, mentioned it in a footnote.[41] Thus the existence of two systems immediately created confusion and potential danger in medical practice. Moss's system was adopted in Britain, France, and US, while Janský's was preferred in most other European countries and some parts of US. It was reported that "The practically universal use of the Moss classification at that time was completely and purposely cast aside. Therefore in place of bringing order out of chaos, chaos was increased in the larger cities."[46] To resolve the confusion, the American Association of Immunologists, the Society of American Bacteriologists, and the Association of Pathologists and Bacteriologists made a joint recommendation in 1921 that the Jansky classification be adopted based on priority.[47] But it was not followed particularly where Moss's system had been used.[48]

In 1927, Landsteiner, who had moved to the Rockefeller Institute for Medical Research in New York, and as a member of a committee of the National Research Council concerned with blood grouping suggested to substitute Janský's and Moss's systems with the letters O, A, B, and AB. There was another confusion on the use of O which was introduced by Polish physicians Ludwik Hirszfeld and German physician Emil von Dungern in 1910.[49] It was never clear whether it was meant for the figure 0, German null for zero or the upper case letter O for ohne, meaning without; Landsteiner chose the latter.[50]

In 1928 the Permanent Commission on Biological Standardization adopted Landsteiner's proposal and stated:

The Commission learns with satisfaction that, on the initiative of the Health Organization of the League of Nations, the nomenclature proposed by von Dungern and Hirszfeld for the classification of blood groups has been generally accepted, and recommends that this nomenclature shall be adopted for international use as follows: 0 A B AB. To facilitate the change from the nomenclature hitherto employed the following is suggested:

  • Jansky ....0(I) A(I1) B(III) AB(IV)
  • Moss ... O(IV) A(II) B(I) AB(l)[51]

This classification became widely accepted; however, not all hospitals and doctors used blood typing for transfusion even in the late 1940s. The new system was gradually accepted and by the early 1950s, it was universally followed.[52]

Hirszfeld and Dungern discovered the inheritance of blood types as Mendelian genetics in 1910 and the existence of sub-types of A in 1911.[49][53] In 1927, Landsteiner, with Philip Levine, discovered the MN blood group system,[54] and the P system.[55] Development of the Coombs test in 1945,[56] the advent of transfusion medicine, and the understanding of ABO hemolytic disease of the newborn led to discovery of more blood groups. As of 2020[update], the International Society of Blood Transfusion (ISBT) recognizes 41 blood groups.[2]

Society and culture[edit]

Main article: Blood type personality theory

A popular pseudoscientific belief in Eastern Asian countries (especially in Japan and Korea; known as 血液型 ketsuekigata / hyeoraekhyeong) is that a person's ABO blood type is predictive of their personality, character, and compatibility with others.[57] Researchers have established no scientific basis exists for blood type personality categorization, and studies have found no "significant relationship between personality and blood type, rendering the theory "obsolete" and concluding that no basis exists to assume that personality is anything more than randomly associated with blood type."[58]

See also[edit]


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  47. ^Garratty, G.; Dzik, W.; Issitt, P. D.; Lublin, D. M.; Reid, M. E.; Zelinski, T. (2000). "Terminology for blood group antigens and genes-historical origins and guidelines in the new millennium". Transfusion. 40 (4): 477–489. doi:10.1046/j.1537-2995.2000.40040477.x. PMID 10773062.
  48. ^Doan, C.A. (1927). "The Transfusion problem". Physiological Reviews. 7 (1): 1–84. doi:10.1152/physrev.1927.7.1.1. ISSN 0031-9333.
  49. ^ abOkroi, Mathias; McCarthy, Leo J. (July 2010). "The original blood group pioneers: the Hirszfelds". Transfusion Medicine Reviews. 24 (3): 244–246. doi:10.1016/j.tmrv.2010.03.006. ISSN 1532-9496. PMID 20656191.
  50. ^Schmidt, P.; Okroi, M. (2001). "Also sprach Landsteiner – Blood Group 'O' or Blood Group 'NULL'". Transfusion Medicine and Hemotherapy. 28 (4): 206–208. doi:10.1159/000050239. ISSN 1660-3796. S2CID 57677644.
  51. ^Goodman, Neville M. (1940). "Nomenclature of Blood Groups". British Medical Journal. 1 (4123): 73. PMC 2176232.
  52. ^Garratty, G.; Dzik, W.; Issitt, P.D.; Lublin, D.M.; Reid, M.E.; Zelinski, T. (2000). "Terminology for blood group antigens and genes-historical origins and guidelines in the new millennium". Transfusion. 40 (4): 477–489. doi:10.1046/j.1537-2995.2000.40040477.x. ISSN 0041-1132. PMID 10773062. S2CID 23291031.
  53. ^Dungern, E.; Hirschfeld, L. (1911). "Über Vererbung gruppenspezifischer Strukturen des Blutes". Zeitschrift für Induktive Abstammungs- und Vererbungslehre (in German). 5 (1): 196–197. doi:10.1007/BF01798027.
  54. ^Landsteiner, K.; Levine, P. (1927). "A New Agglutinable Factor Differentiating Individual Human Bloods". Experimental Biology and Medicine. 24 (6): 600–602. doi:10.3181/00379727-24-3483. S2CID 87597493.
  55. ^Landsteiner, K.; Levine, P. (1927). "Further Observations on Individual Differences of Human Blood". Experimental Biology and Medicine. 24 (9): 941–942. doi:10.3181/00379727-24-3649. S2CID 88119106.
  56. ^Coombs RR, Mourant AE, Race RR (1945). "A new test for the detection of weak and incomplete Rh agglutinins". Br J Exp Pathol. 26: 255–66. PMC 2065689. PMID 21006651.
  57. ^Nuwer, Rachel. "You are what you bleed: In Japan and other east Asian countries some believe blood type dictates personality". Scientific American. Retrieved 16 Feb 2011.
  58. ^"Despite scientific debunking, in Japan you are what your blood type is". MediResource Inc. Associated Press. 2009-02-01. Archived from the original on September 28, 2011. Retrieved 2011-08-13.

Further reading[edit]

External links[edit]

  • BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH has details of genes and proteins, and variations thereof, that are responsible for blood types
  • Online Mendelian Inheritance in Man (OMIM): ABO Glycosyltransferase; ABO - 110300
  • Online Mendelian Inheritance in Man (OMIM): Rhesus Blood Group, D Antigen; RHD - 111680
  • "Blood group test". Gentest.ch GmbH. Archived from the original on 2017-03-24. Retrieved 2017-03-23.
  • "Blood Facts – Rare Traits". LifeShare Blood Centers. Archived from the original on September 26, 2006. Retrieved September 15, 2006.
  • "Modern Human Variation: Distribution of Blood Types". Dr. Dennis O'Neil, Behavioral Sciences Department, Palomar College, San Marcos, California. 2001-06-06. Archived from the original on 2001-06-06. Retrieved November 23, 2006.
  • "Racial and Ethnic Distribution of ABO Blood Types – BloodBook.com, Blood Information for Life". bloodbook.com. Archived from the original on 2010-03-04. Retrieved September 15, 2006.
  • "Molecular Genetic Basis of ABO". Retrieved July 31, 2008.
Sours: https://en.wikipedia.org/wiki/Blood_type
Why do we have different BLOOD GROUPS? Why Do we need Blood Transfusion?

A Brief History of Human Blood Groups

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ABO blood group system

Classification of blood types

"ABO" redirects here. For other uses, see ABO (disambiguation).

"Type O" redirects here. It is not to be confused with Typo or Type 0.

The ABO blood group system is used to denote the presence of one, both, or neither of the A and B antigens on erythrocytes.[1] In human blood transfusions it is the most important of the 38 different blood type (or group) classification systems currently recognized.[2] A mismatch (very rare in modern medicine) in this, or any other serotype, can cause a potentially fatal adverse reaction after a transfusion, or an unwanted immune response to an organ transplant.[3] The associated anti-A and anti-B antibodies are usually IgM antibodies, produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses.

The ABO blood types were discovered by Karl Landsteiner in 1901; he received the Nobel Prize in Physiology or Medicine in 1930 for this discovery.[4] ABO blood types are also present in other primates such as apes and Old World monkeys.[5]



The ABO blood types were first discovered by an Austrian Physician Karl Landsteiner working at the Pathological-Anatomical Institute of the University of Vienna (now Medical University of Vienna). In 1900, he found that red blood cells would clump together (agglutinate) when mixed in test tubes with sera from different persons, and that some human blood also agglutinated with animal blood.[6] He wrote a two-sentence footnote:

The serum of healthy human beings not only agglutinates animal red cells, but also often those of human origin, from other individuals. It remains to be seen whether this appearance is related to inborn differences between individuals or it is the result of some damage of bacterial kind.[7]

This was the first evidence that blood variations exist in humans – it was believed that all humans have similar blood. The next year, in 1901, he made a definitive observation that blood serum of an individual would agglutinate with only those of certain individuals. Based on this he classified human blood into three groups, namely group A, group B, and group C. He defined that group A blood agglutinates with group B, but never with its own type. Similarly, group B blood agglutinates with group A. Group C blood is different in that it agglutinates with both A and B.[8]

This was the discovery of blood groups for which Landsteiner was awarded the Nobel Prize in Physiology or Medicine in 1930. In his paper, he referred to the specific blood group interactions as isoagglutination, and also introduced the concept of agglutinins (antibodies), which is the actual basis of antigen-antibody reaction in the ABO system.[9] He asserted:

[It] may be said that there exist at least two different types of agglutinins, one in A, another one in B, and both together in C. The red blood cells are inert to the agglutinins which are present in the same serum.[8]

Thus, he discovered two antigens (agglutinogens A and B) and two antibodies (agglutinins - anti-A and anti-B). His third group (C) indicated absence of both A and B antigens, but contains anti-A and anti-B.[9] The following year, his students Adriano Sturli and Alfred von Decastello discovered the fourth type (but not naming it, and simply referred to it as "no particular type").[10][11]

Ukrainemarine uniform imprint, showing the wearer's blood type as "B (III) Rh+".

In 1910, Ludwik Hirszfeld and Emil Freiherr von Dungern introduced the term O (null) for the group Landsteiner designated as C, and AB for the type discovered by Sturli and von Decastello. They were also the first to explain the genetic inheritance of the blood groups.[12][13]

Classification systems[edit]

Jan Janský, who invented type I, II, III, IV system.

Czech serologist Jan Janský independently introduced blood type classification in 1907 in a local journal.[14] He used the Roman numerical I, II, III, and IV (corresponding to modern O, A, B, and AB). Unknown to Janský, an American physician William L. Moss devised a slightly different classification using the same numerical;[15] his I, II, III, and IV corresponding to modern AB, A, B, and O.[11]

These two systems created confusion and potential danger in medical practice. Moss's system was adopted in Britain, France, and US, while Janský's was preferred in most European countries and some parts of US. To resolve the chaos, the American Association of Immunologists, the Society of American Bacteriologists, and the Association of Pathologists and Bacteriologists made a joint recommendation in 1921 that the Jansky classification be adopted based on priority.[16] But it was not followed particularly where Moss's system had been used.[17]

In 1927, Landsteiner, who had moved to the Rockefeller Institute for Medical Research in New York, and as a member of a committee of the National Research Council concerned with blood grouping suggested to substitute Janský's and Moss's systems with the letters O, A, B, and AB. (There was another confusion on the use of figure 0 for German null as introduced by Hirszfeld and von Dungern, because others used the letter O for ohne, meaning without or zero; Landsteiner chose the latter.[17]) This classification was adopted by the National Research Council and became variously known as the National Research Council classification, the International classification, and most popularly the "new" Landsteiner classification. The new system was gradually accepted and by the early 1950s, it was universally followed.[18]

Other developments[edit]

The first practical use of blood typing in transfusion was by an American physician Reuben Ottenberg in 1907. And the large-scale application started during the First World War (1914-1915) when citric acid was developed as blood clot prevention.[9]Felix Bernstein demonstrated the correct blood group inheritance pattern of multiple alleles at one locus in 1924.[19] Watkins and Morgan, in England, discovered that the ABO epitopes were conferred by sugars, to be specific, N-acetylgalactosamine for the A-type and galactose for the B-type.[20][21][22] After much published literature claiming that the ABH substances were all attached to glycosphingolipids, Finne et al. (1978) found that the human erythrocyte glycoproteins contain polylactosamine chains[23] that contains ABH substances attached and represent the majority of the antigens.[24][25][26] The main glycoproteins carrying the ABH antigens were identified to be the Band 3 and Band 4.5 proteins and glycophorin.[27] Later, Yamamoto's group showed the precise glycosyl transferase set that confers the A, B and O epitopes.[28]

Diagram showing the carbohydrate chains that determine the ABO blood group

Student blood test. Three drops of blood are mixed with anti-B (left) and anti-A (right) serum. Agglutination on the right side indicates blood type A.

There are three basic variants of immunoglobulin antigens in humans that share a very similar chemical structure but are distinctly different. Red circles show where there are differences in chemical structure in the antigen-binding site (sometimes called the antibody-combining site) of human immunoglobulin. Notice the O-type antigen does not have a binding site.[29]


Blood groups are inherited from both parents. The ABO blood type is controlled by a single gene (the ABO gene) with three types of alleles inferred from classical genetics: i, IA, and IB. The I designation stands for isoagglutinogen, another term for antigen.[30] The gene encodes a glycosyltransferase—that is, an enzyme that modifies the carbohydrate content of the red blood cell antigens. The gene is located on the long arm of the ninth chromosome (9q34).[citation needed]

The IA allele gives type A, IB gives type B, and i gives type O. As both IA and IB are dominant over i, only ii people have type O blood. Individuals with IAIA or IAi have type A blood, and individuals with IBIB or IBi have type B. IAIB people have both phenotypes, because A and B express a special dominance relationship: codominance, which means that type A and B parents can have an AB child. A couple with type A and type B can also have a type O child if they are both heterozygous (IBi,IAi). The cis-AB phenotype has a single enzyme that creates both A and B antigens. The resulting red blood cells do not usually express A or B antigen at the same level that would be expected on common group A1 or B red blood cells, which can help solve the problem of an apparently genetically impossible blood group.[31]

Blood group inheritance
Blood type OABAB
O or A
O or B
A or B
AIAi(AO)O or A
O or A
O, A, B or AB
B or AB
A, B or AB
A or AB
A or AB
BIBi(BO)O or B
O, A, B or AB
A or AB
O or B
A, B or AB
B or AB
B or AB
A, B or AB
A or AB
A, B or AB
B or AB
A, B, or AB

The table above summarizes the various blood groups that children may inherit from their parents.[32][33] Genotypes are shown in the second column and in small print for the offspring: AO and AA both test as type A; BO and BB test as type B. The four possibilities represent the combinations obtained when one allele is taken from each parent; each has a 25% chance, but some occur more than once. The text above them summarizes the outcomes.

Blood group inheritance by phenotype only
Blood type OABAB
OO O or A O or B A or B
AO or A O or A O, A, B or AB A, B or AB
BO or B O, A, B or AB O or B A, B or AB
ABA or B A, B or AB A, B or AB A, B or AB

Historically, ABO blood tests were used in paternity testing, but in 1957 only 50% of American men falsely accused were able to use them as evidence against paternity.[34] Occasionally, the blood types of children are not consistent with expectations—for example, a type O child can be born to an AB parent—due to rare situations, such as Bombay phenotype and cis AB.[35]


The A blood type contains about 20 subgroups, of which A1 and A2 are the most common (over 99%). A1 makes up about 80% of all A-type blood, with A2 making up almost all of the rest.[36] These two subgroups are not always interchangeable as far as transfusion is concerned, as some A2 individuals produce antibodies against the A1 antigen. Complications can sometimes arise in rare cases when typing the blood.[36]

With the development of DNA sequencing, it has been possible to identify a much larger number of alleles at the ABO locus, each of which can be categorized as A, B, or O in terms of the reaction to transfusion, but which can be distinguished by variations in the DNA sequence. There are six common alleles in white individuals of the ABO gene that produce one's blood type:[37][38]

A101 (A1)
A201 (A2)
B101 (B1) O01 (O1)
O02 (O1v)
O03 (O2)

The same study also identified 18 rare alleles, which generally have a weaker glycosylation activity. People with weak alleles of A can sometimes express anti-A antibodies, though these are usually not clinically significant as they do not stably interact with the antigen at body temperature.[39]

Cis AB is another rare variant, in which A and B genes are transmitted together from a single parent.

Distribution and evolutionary history[edit]

Main article: Blood type distribution by country

The distribution of the blood groups A, B, O and AB varies across the world according to the population. There are also variations in blood type distribution within human subpopulations.[citation needed]

In the UK, the distribution of blood type frequencies through the population still shows some correlation to the distribution of placenames and to the successive invasions and migrations including Celts, Norsemen, Danes, Anglo-Saxons, and Normans who contributed the morphemes to the placenames and the genes to the population. The native Celts tended to have more type O blood, while the other populations tended to have more type A.[40]

The two common O alleles, O01 and O02, share their first 261 nucleotides with the group A allele A01.[41] However, unlike the group A allele, a guanosine base is subsequently deleted. A premature stop codon results from this frame-shift mutation. This variant is found worldwide, and likely predates human migration from Africa. The O01 allele is considered to predate the O02 allele.[citation needed]

Some evolutionary biologists theorize that there are four main lineages of the ABO gene and that mutations creating type O have occurred at least three times in humans.[42] From oldest to youngest, these lineages comprise the following alleles: A101/A201/O09, B101, O02 and O01. The continued presence of the O alleles is hypothesized to be the result of balancing selection.[42] Both theories contradict the previously held theory that type O blood evolved first.[citation needed]

Origin theories[edit]

It is possible that food and environmental antigens (bacterial, viral, or plant antigens) have epitopes similar enough to A and B glycoprotein antigens. The antibodies created against these environmental antigens in the first years of life can cross-react with ABO-incompatible red blood cells that it comes in contact with during blood transfusion later in life. Anti-A antibodies are hypothesized to originate from immune response towards influenza virus, whose epitopes are similar enough to the α-D-N-galactosamine on the A glycoprotein to be able to elicit a cross-reaction. Anti-B antibodies are hypothesized to originate from antibodies produced against Gram-negative bacteria, such as E. coli, cross-reacting with the α-D-galactose on the B glycoprotein.[43]

However, it is more likely that the force driving evolution of allele diversity is simply negative frequency-dependent selection; cells with rare variants of membrane antigens are more easily distinguished by the immune system from pathogens carrying antigens from other hosts. Thus, individuals possessing rare types are better equipped to detect pathogens. The high within-population diversity observed in human populations would, then, be a consequence of natural selection on individuals.[44]

Clinical relevance[edit]

The carbohydrate molecules on the surfaces of red blood cells have roles in cell membrane integrity, cell adhesion, membrane transportation of molecules, and acting as receptors for extracellular ligands, and enzymes. ABO antigens are found having similar roles on epithelial cells as well as red blood cells.[45][46]

Bleeding and thrombosis (von Willebrand factor)[edit]

The ABO antigen is also expressed on the von Willebrand factor (vWF) glycoprotein,[47] which participates in hemostasis (control of bleeding). In fact, having type O blood predisposes to bleeding,[48] as 30% of the total genetic variation observed in plasma vWF is explained by the effect of the ABO blood group,[49] and individuals with group O blood normally have significantly lower plasma levels of vWF (and Factor VIII) than do non-O individuals.[50][51] In addition, vWF is degraded more rapidly due to the higher prevalence of blood group O with the Cys1584 variant of vWF (an amino acid polymorphism in VWF):[52] the gene for ADAMTS13 (vWF-cleaving protease) maps to human chromosome 9 band q34.2, the same locus as ABO blood type. Higher levels of vWF are more common amongst people who have had ischemic stroke (from blood clotting) for the first time.[53] The results of this study found that the occurrence was not affected by ADAMTS13 polymorphism, and the only significant genetic factor was the person's blood group.[citation needed]

ABO hemolytic disease of the newborn[edit]

Main article: Hemolytic disease of the newborn (ABO)

ABO blood group incompatibilities between the mother and child does not usually cause hemolytic disease of the newborn (HDN) because antibodies to the ABO blood groups are usually of the IgM type, which do not cross the placenta. However, in an O-type mother, IgG ABO antibodies are produced and the baby can potentially develop ABO hemolytic disease of the newborn.[citation needed]

Clinical applications[edit]

In human cells, the ABO alleles and their encoded glycosyltransferases have been described in several oncologic conditions.[54] Using anti-GTA/GTB monoclonal antibodies, it was demonstrated that a loss of these enzymes was correlated to malignant bladder and oral epithelia.[55][56] Furthermore, the expression of ABO blood group antigens in normal human tissues is dependent the type of differentiation of the epithelium. In most human carcinomas, including oral carcinoma, a significant event as part of the underlying mechanism is decreased expression of the A and B antigens.[57] Several studies have observed that a relative down-regulation of GTA and GTB occurs in oral carcinomas in association with tumor development.[57][58] More recently, a genome wide association study (GWAS) has identified variants in the ABO locus associated with susceptibility to pancreatic cancer.[59]

Clinical marker[edit]

A multi-locus genetic risk score study based on a combination of 27 loci, including the ABO gene, identified individuals at increased risk for both incident and recurrent coronary artery disease events, as well as an enhanced clinical benefit from statin therapy. The study was based on a community cohort study (the Malmo Diet and Cancer study) and four additional randomized controlled trials of primary prevention cohorts (JUPITER and ASCOT) and secondary prevention cohorts (CARE and PROVE IT-TIMI 22).[60]

Alteration of ABO antigens for transfusion[edit]

In April 2007, an international team of researchers announced in the journal Nature Biotechnology an inexpensive and efficient way to convert types A, B, and AB blood into type O.[61] This is done by using glycosidase enzymes from specific bacteria to strip the blood group antigens from red blood cells. The removal of A and B antigens still does not address the problem of the Rh blood group antigen on the blood cells of Rh positive individuals, and so blood from Rh negative donors must be used. The sort of blood is named "enzyme converted to O" (ECO) blood. Patient trials will be conducted before the method can be relied on in live situations. One such Phase II trial was done on B-to-O blood in 2002.[62]

Another approach to the blood antigen problem is the manufacture of artificial blood, which could act as a substitute in emergencies.[63]


Main article: Blood type personality theory

During the 1930s, connecting blood groups to personality types became popular in Japan and other areas of the world.[64] Studies of this association have yet to confirm its existence definitively.[65]

Other popular but unsupported ideas include the use of a blood type diet, claims that group A causes severe hangovers, group O is associated with perfect teeth, and those with blood group A2 have the highest IQs. Scientific evidence in support of these concepts is limited at best.[66]

See also[edit]


  1. ^The Editors of Encyclopædia Britannica (18 July 2017). "ABO blood group system". Encyclopædia Britannica. Encyclopædia Britannica, Inc. Retrieved 26 October 2017.
  2. ^Storry, J. R.; Castilho, L.; Chen, Q.; Daniels, G.; Denomme, G.; Flegel, W. A.; Gassner, C.; de Haas, M.; et al. (2016). "International society of blood transfusion working party on red cell immunogenetics and terminology: report of the Seoul and London meetings". ISBT Science Series. 11 (2): 118–122. doi:10.1111/voxs.12280. ISSN 1751-2816. PMC 5662010. PMID 29093749.
  3. ^Muramatsu M, Gonzalez HD, Cacciola R, Aikawa A, Yaqoob MM, Puliatti C (2014). "ABO incompatible renal transplants: Good or bad?". World Journal of Transplantation. 4 (1): 18–29. doi:10.5500/wjt.v4.i1.18. ISSN 2220-3230. PMC 3964193. PMID 24669364.
  4. ^Maton, Anthea; Jean Hopkins; Charles William McLaughlin; Susan Johnson; Maryanna Quon Warner; David LaHart; Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN .
  5. ^Segurel, L.; Thompson, E. E.; Flutre, T.; Lovstad, J.; Venkat, A.; Margulis, S. W.; Moyse, J.; Ross, S.; Gamble, K.; Sella, G.; Ober, C. (2012). "The ABO blood group is a trans-species polymorphism in primates". Proceedings of the National Academy of Sciences. 109 (45): 18493–18498. arXiv:1208.4613. Bibcode:2012PNAS..10918493S. doi:10.1073/pnas.1210603109. PMC 3494955. PMID 23091028.
  6. ^Landsteiner K (1900). "Zur Kenntnis der antifermentativen, lytischen und agglutinierenden Wirkungen des Blutserums und der Lymphe". Zentralblatt für Bakteriologie, Parasitenkunde und Infektionskrankheiten. 27: 357–362.
  7. ^Kantha, S.S. (1995). "The blood revolution initiated by the famous footnote of Karl Landsteiner's 1900 paper"(PDF). The Ceylon Medical Journal. 40 (3): 123–125. PMID 8536328.
  8. ^ abLandsteiner, Karl (1961) [1901]. "On Agglutination of Normal Human Blood". Transfusion. 1 (1): 5–8. doi:10.1111/j.1537-2995.1961.tb00005.x. ISSN 0041-1132. PMID 13758692. S2CID 40158397Originally published in German in Wiener Klinische Wochenschrift, 46, 1132–1134CS1 maint: postscript (link)
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Further reading[edit]

External links[edit]

Sours: https://en.wikipedia.org/wiki/ABO_blood_group_system

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