The isoantibodies anti-A and anti-B which are described differ in several respects from those occurring in normal human serum. This type of antibody has first been observed in the serum of an Rh negative woman who exhibited a history of erythroblastosis. Her husband belonged to the subtype Rh1 and to the blood group A. The patient’s serum completely neutralized with A and B substances still agglutinated strongly the husband’s cells provided normal human serum replaced physiological saline solution as a diluent for all dilutions. The impression was thus created that an Rh blocking antibody was responsible for the agglutination observed. It could be shown, however, that the abnormal antibody present in this patient’s serum was not an Rh antibody at all but instead, an antibody directed against the A property. This type of anti-A antibody resembles the Rh blocking antibody in many respects. It becomes manifest only if undiluted human serum is used as a diluent. Surprisingly enough this antibody agglutinated cells of group A, although the amount of AB substances added to the serum was sufficient to neutralize completely the isoagglutinin anti-A under normal conditions in which saline solution is used as a diluent. This anti-A antibody therefore cannot be neutralized as easily as the normal isoagglutinin anti-A. For its neutralization much larger amounts of the blood group specific substances are apparently necessary. The patient’s serum fixed complement when mixed with material containing water soluble A substance, in contrast to the normal isoantibody anti-A which failed to do so. The titer of isoantibodies found in the patient’s serum upon titration in saline solution was not extensively high and, as a matter of fact, was average. It is therefore felt that an extremely high titer is neither a necessary requirement nor proof of isoimmunization toward the A and B factors. Another interesting characteristic of the peculiar anti-A antibody occurring in our patient’s serum was the fact that it was essentially an anti-A1 antibody. The difference in agglutination between A1 and A2 cells respectively becomes manifest if normal serum is used as a diluent instead of saline solution. This difference becomes even more marked after neutralization of the patient’s serum with A and B substances.

During the course of Mrs. Bong’s pregnancy the special anti-A antibody described did not increase but rather decreased in strength. However, even after delivery the antibody was demonstrable for at least several weeks although we had no opportunity to examine the patient’s serum further. That one must be very careful in contributing any pathological significance to isoantibodies anti-A or anti-B, even of the type described, is evident from the fact that the patient was delivered of a perfectly normal baby belonging to the blood group O and being Rh negative. Whether the difficulties experienced by the patient in previous pregnancies were due to sensitization toward the Rh factor or to the A factor cannot be decided.

Antibodies anti-A and anti-B of the type reported were also found in the sera of patients who had received large amounts of pooled plasma or O blood conditioned with A and B specific substances. Again the anti-A antibody occurring in the serum of these patients was mainly directed against the A1 property. Under the experimental conditions described in this paper, such a serum can be used for the differential diagnosis of the subgroups A1 and A2 and constitutes a sensitive reagent for the recognition of the differences occurring within the A factor. With the aid of such a serum only 10 per cent of A cells were found to belong to subgroup A2, 75 per cent to A1, and 15 per cent were considered to be of the intermediate type. No subgroups were found so far in human cells of group B.

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