physiologist Karl Landsteiner. After experimenting with mixing the blood of his laboratory dogs and observing their cross-reactions, he began his work on humans. He mixed the blood of several different individuals together and noticed that sometimes when he did this the red blood cells stuck together in a clump. This did not happen every time, but only with certain combinations of individuals. If this red-cell clumping was occurring in transfused patients, the blood would virtually solidify, which would explain the fatal reaction. It also explained why some patients tolerated a transfusion and showed no signs at all of a reaction.
Landsteiner interpreted the results of his mixing experiments by suggesting that people belonged to one of the three blood groups, A, B or O. Two years later a fourth group, AB, was discovered. This also explained the erratic pattern of transfusion complications. Giving a group A patient a transfusion of blood from a group A donor was fine; tranfuse a group A patient with blood from a group B donor and there would be trouble. But so long as the donor and patient blood groups were the same there was no problem.
It took a few years to discover the chemical basis for the different types of blood. The blood groups are the result of a simple genetic difference that occurs on the surface of red blood cells, the cells that carry oxygen and give blood its colour. On the outside of each red blood cell sits a molecule that can occur in two very slightly different forms, A or B. People in group A have, unsurprisingly, version A on the surface of their red cells while in group B, this is replacedby version B. In the rare AB group the cells have both A and B versions on their outer surface. People in group O have neither A nor B versions of the molecule. Their red cells are, in a sense, bald.
But these slight differences, which don’t affect the efficiency or the working of the cells at all, are not on their own sufficient to cause trouble on transfusion. The problem arises because, after a few months outside the womb, the blood serum begins to build up antibodies to the
opposite
version of the molecule on their own cells. People in group A build up anti-B antibodies in their serum. Again, this does not interfere with normal everyday life. People never make antibodies to their own blood cells, so people in group A don’t make anti-A antibodies, only anti-B. Since people with blood group AB have both versions on their red cells, they make neither anti-A nor anti-B antibodies while, for the same reason, people in group O, whose cells have neither A nor B, are free to make both anti-A and anti-B antibodies and they do.
The potentially fatal coagulation reaction occurs when the molecule meets its antibody. They stick to each other like glue and, what is worse, bind all the red cells into a sticky clump, the cause of all the trouble in mismatched transfusions. That’s why no one makes antibodies against their own cells. They would coagulate their own red blood cells and die.
Under normal circumstances blood cells never encounter their own antibodies, but transfusion opens up that possibility. Transfuse a group A patient with blood from a group B donor and the antibodies will play havoc. Two thingshappen. The group B cells from the donor are coagulated by the anti-B in the patient’s serum and the anti-A in the donor’s serum clumps the patient’s own cells. Group O blood is really bad news because its serum contains both anti-A
and
anti-B which will attach the cells of any other blood group. However, as good methods were developed to separate the donor’s cells from the liquid serum, things got a bit easier. Group O cells, separated then rinsed free of antibody-containing serum, can be transfused into any patient, and if red cells are all you need that’s fine. Group O is the universal red-cell donor, as long as you wash them thoroughly first to remove the serum antibodies. If you need serum, not cells,
Landsteiner interpreted the results of his mixing experiments by suggesting that people belonged to one of the three blood groups, A, B or O. Two years later a fourth group, AB, was discovered. This also explained the erratic pattern of transfusion complications. Giving a group A patient a transfusion of blood from a group A donor was fine; tranfuse a group A patient with blood from a group B donor and there would be trouble. But so long as the donor and patient blood groups were the same there was no problem.
It took a few years to discover the chemical basis for the different types of blood. The blood groups are the result of a simple genetic difference that occurs on the surface of red blood cells, the cells that carry oxygen and give blood its colour. On the outside of each red blood cell sits a molecule that can occur in two very slightly different forms, A or B. People in group A have, unsurprisingly, version A on the surface of their red cells while in group B, this is replacedby version B. In the rare AB group the cells have both A and B versions on their outer surface. People in group O have neither A nor B versions of the molecule. Their red cells are, in a sense, bald.
But these slight differences, which don’t affect the efficiency or the working of the cells at all, are not on their own sufficient to cause trouble on transfusion. The problem arises because, after a few months outside the womb, the blood serum begins to build up antibodies to the
opposite
version of the molecule on their own cells. People in group A build up anti-B antibodies in their serum. Again, this does not interfere with normal everyday life. People never make antibodies to their own blood cells, so people in group A don’t make anti-A antibodies, only anti-B. Since people with blood group AB have both versions on their red cells, they make neither anti-A nor anti-B antibodies while, for the same reason, people in group O, whose cells have neither A nor B, are free to make both anti-A and anti-B antibodies and they do.
The potentially fatal coagulation reaction occurs when the molecule meets its antibody. They stick to each other like glue and, what is worse, bind all the red cells into a sticky clump, the cause of all the trouble in mismatched transfusions. That’s why no one makes antibodies against their own cells. They would coagulate their own red blood cells and die.
Under normal circumstances blood cells never encounter their own antibodies, but transfusion opens up that possibility. Transfuse a group A patient with blood from a group B donor and the antibodies will play havoc. Two thingshappen. The group B cells from the donor are coagulated by the anti-B in the patient’s serum and the anti-A in the donor’s serum clumps the patient’s own cells. Group O blood is really bad news because its serum contains both anti-A
and
anti-B which will attach the cells of any other blood group. However, as good methods were developed to separate the donor’s cells from the liquid serum, things got a bit easier. Group O cells, separated then rinsed free of antibody-containing serum, can be transfused into any patient, and if red cells are all you need that’s fine. Group O is the universal red-cell donor, as long as you wash them thoroughly first to remove the serum antibodies. If you need serum, not cells,
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