Abstract
A blood specimen from a normal male donor was found to have both type A1, MNS and O, Ns cells. Gross physical examination, chromosome analysis, bilateral dermatoglyphic comparisons, blood grouping and secretor studies lead to the conclusion that interfetal transplantation of erythropoietic tissue is the most likely basis for the state of blood chimerism in this individual. Unlike other well-documented examples of human blood group chimerism there is no co-twin. However, a strong history of twinning in the family, a pair of fraternal twins among the sibs and a neonatal history of low birth weight but full maturity indicates that the individual may have been a twin. It is postulated that a co-twin died and was absorbed in early fetal life.
Another unusual feature of the case is the persistence of anti-A isoagglutinins in the type O host despite the A1 transplant. The isoagglutinin reacts at body temperatures with the product in another sib of the A gene responsible for the transplanted A antigen. There is γ-globulin, predominantly γM, on the transplanted cell surfaces, but there is no evidence of accelerated blood production or destruction. Quantitative studies of the transplanted A antigen reveals it to be greatly reduced in potency but qualitatively of type A1; its H is possibly enhanced and qualitatively like that of type O.
Because of the contradictory immunologic features in this case, consideration is given to unusual mechanisms of tolerance which might permit a transplant to survive in the presence of specific antibody. The favored hypothesis is that multivalent binding of iso-antibody molecules to multiple antigenic sites on single red cells is involved. This type of complexing could account for the reduction in antigen strength yet normal red cell survival. The data presented are also consistent with the possibility of biochemical modification of the transplant cell’s antigens. This is indicated not only by attenuation of its A antigen but also by suggestive augmentation of its H antigen. Considerations are given to how such modification could be mediated serologically by host antibody.
To date, central inhibition of erythrocyte isoagglutinin production has been the implied mechanism responsible for transplant compatibility in cases of both bovine and human blood group chimerism. Nevertheless, in this case, whatever the mechanism might be, central inhibition of antibody to at least one of the transplant’s antigens is not operating. Therefore, human blood group chimerism may be achieved by means other than that of classic immunologic tolerance; otherwise A B O antigens would have to be considered as other than transplant antigens.
