The serum of a 39-year-old male under long-term platelet transfusion therapy for hypoplastic anemia with thrombocytopenia was investigated for the presence of leukocyte and platelet antibodies after the patients had received platelet concentrates from more than 700 random donors. The serological studies of his serum revealed: (1) the absence of platelet-reactive antibodies; (2) the absence of agglutinating or cytotoxic antibodies against leukocytes; (3) the presence of at least two granulocyte-specific antibodies, one with the specificity anti-NA2 and the other with an undefined specificity, both only detectable by indirect immunofluorescence, and (4) the presence of cytotoxic-negative fluorescence-positive peripheral-blood-mononuclear-cell-reactive antibodies, not directed against HLA-A, B or C antigens. The significance and implications of these findings are briefly discussed.

Two hundred and eight pregnancy sera were tested for the presence of antibodies specific for lymphocyte sub‐populations by using the isolated B and T lymphocytes from the women's mating partners. This was done by the microlymphocytotoxicity and the indirect immuno‐fluorescence techniques. Five sera (2.5%) reacted exclusively with B lymphocytes and sixty‐three sera (30.2%) reacted with both B and T lymphocytes; none of the sera was specific for T cells. Several sera, reacting with both B and T lymphocytes, were absorbed with platelets and this procedure revealed nine additional antisera specific for B lymphocyte antigens. Specificity studies on a panel of forty‐eight HLA—ABCD typed individuals indicated that most antisera possibly defined new B‐cell antigens. Family studies established that the antigens defined by these antisera were coded for by genes in the Major Histocompatibility Complex.

The serum of a 39-year-old male under long-term platelet transfusion therapy for hypoplastic anemia with thrombocytopenia was investigated for the presence of leukocyte and platelet antibodies after the patient had received platelet concentrates from more than 700 random donors. The serological studies of his serum revealed: (1) the absence of plateletreactive antibodies ; (2) the absence of agglutinating or cytotoxic antibodies against leukocytes ; (3) the presence of at least two granulocyte-specific antibodies, one with the specificity anti- NA(2) and the other with an undefined specificity, both only detectable by indirect immunofluorescence, and (4) the presence of cytotoxic-negative fluorescence-positive peripheral-bloodmononuclear- cell-reactive antibodies, not directed against HLA-A, B or C antigens. The significance and implications of these findings are briefly discussed.

During the VIIth Histocompatibility Workshop, 44 sera were selected that defined B-cell alloantigens showing correlation with the HLA-D antigenic determinants. The segregation of these antigens, now called DRw (HLA-D-related), was studied in a family that contained one HLA-A/B recombinant and one HLA-B/D recombinant sibling. I t could be established that the DRw-1 antigenic determinants segregated with the B-D region in the AIB recombinant sibling and that the DRw-2 antigen segregated with the D region of the B/D recombinant child. In the second family, DRw typing showed that one of the children was identical with an HLA-ABC non-identical sibling. This suggested that a crossing-over had occurred. This was confirmed by mutual non-stimulation of these HLA-ABC non-identical children in the mixed lymphocyte culture. This crossing-over involved the DRw-3 alloantigen.These data confirm the assumption that serologically defined B-cell alloantigens are coded for by genes located outside the HLA-A/B region on the B-D side of the chromosome. Moreover, these data suggest that, within families, serological B-cell genotype identity can predict a mutual unresponsiveness in the lymphocyte culture.However, findings in these two families indicate that discrepancies nevertheless exist between B-cell serology and mixed lymphocyte reactions and that mutual stimulation can occur despite apparent identity of serological B-cell phenotype and that B-cell phenotype identity does not necessarily predict mutual unresponsiveness in the mixed lymphocyte culture.