Flossie Cohen

Adenosine-deaminase deficiency in two patients with severely impaired cellular immunity.

Abstract Two young unrelated girls with similar but not identical manifestations of immunological deficiency were found to have no measurable adenosine-deaminase (A.D.A.) enzyme activity in their red blood-cells. The red-cell A.D.A. levels in the parents of one child were about half normal and in the other set of parents about two-thirds normal, suggesting they may be heterozygous, and their affected children homozygous, for a mutant A.D.A. gene. Since the A.D.A. produced by normal lymphocytes is mainly the kind found in red cells, a causal association is postulated between the absence of A.D.A. and impaired lymphocyte function in certain patients with inherited immune disease. An alternative possibility of partial chromosomal deletion is also considered.

Interrelationship of the Various Subgroups of the Blood Group A: Study with Immunofluorescence

The various subgroups of A studied with immunofluorescence seemed to form a single antigenic continuum with the A1 bloods at one end, and the “weak” A bloods at the other. Within this continuum each blood except the strongest samples of A1 was characterized by its own individual spectrum of reactivity, which ranged frcm 4+ to no fluorescence. These findings support a quantitative basis for the differences between the various subgroups of A.

Interrelationship of erythrocyte blood group substances A,B, and H studied with immunofluorescence.

Summary. Adult O cells generally showed strong anti‐H reactions; A cells showed an inverse relationship between A and H reactivity; B cells often lacked the expected inverse relationship, showing both weak and strong anti‐H reactions. Newborn O cells usually reacted weakly with anti‐H; A cells generally lacked a reciprocal relationship, and reacted weakly with both anti‐A and anti‐H; B cells reacted strongly with anti‐B and weakly with anti‐H. All this suggests a special property of B that produces strong reactions regardless of the number of antigenic molecules. Seemingly, the high reactivity of the B antigen accounts for the behavioral divergence between erythrocytes and soluble substances. The findings in groups A, 4B, and O support the Watleins and Morgan theory.

Rh hemolytic disease in ABO-incompatible offspring: Observations on the protective effect of heterospecific pregnancy

Abstract Heterospecific pregnancy is generally believed to protect the mother against Rh sensitization and not to protect the child against Rh hemolytic disease. This study shows that: (1) Rh hemolytic disease was less severe in 126 infants ABO incompatible with their mothers than in 366 compatible infants. The 126 included 53 with combined Rh and ABO hemolytic disease and 73 with only Rh hemolytic disease. Since the height of the maternal Rh titer was not solely responsible for the mildness, it is suggested that possibly Rh antibody is retained in the placenta and related to the binding of anti-A or -B. (2) The sensitization caused by heterospecific pregnancy in 22 per cent of the mothers analyzed showed low titer Rh antibody, which indicates only partial protection by heterospecific pregnancy.

Maternal Rh Antibody and Delayed Neonatal Expression of Rh Antigen

For more than five months after delivery, delay in Rh reactivity was observed in a type A Rh‐positive infant who had received six intrauterine transfusions of type O Rh‐negative blood. The A reaction of the infants erythrocytes was used as a marker for these studies, and delay in the development of Rh reactivity coincided roughly with the period when Rh antibody was demonstrable in the infants serum. Neither “blocking” of Rh receptors nor “dilution” of the infants cells with transfused Rh‐negative cells could be proven to be responsible for the findings, and suppression of Rh antigen by maternal Rh antibody appears to account for the observed phenomenon.