Characterization of HLA-B*3921 and confirmation of HLA-B*4415, two variant HLA-B alleles identified in the Omani population.

We describe a variant HLA-B*39 allele present in two individuals from Oman, which has been officially named HLA-B*3921. In addition we confirm the existence of HLA-B*4415, an allele closely related to HLA-B*4501 differing only at the Bw4/Bw6 epitope.

HLA antigens in an Omani population with dilated cardiomyopathy.

We have investigated the frequency of HLA antigens in 50 Omanis with idiopathic dilated cardiomyopathy to establish whether there are ethnic/racial differences in the reported HLA associations with this disease. There were no statistically significant HLA-A, B, C, DR or DQ antigen frequency differences between the patients and 247 healthy Omanis. THe reported association of HLA-DR4 with idiopathic dilated cardiomyopathy in the Caucasian population does not apply to the Omanis. This confirms the heterogeneity of this disease and points to ethnic/racial origins as important factors when examining the HLA association. This is particularly pertinent as HLD-DR4 has been strongly linked to autoantibody formation in idiopathic dilated cardiomyopathy in Caucasians. The lack of any HLA antigen association in Omanis would argue against the proposed HLA-linked autoimmune pathology of idiopathic dilated cardiomyopathy.

Lymphocytotoxins in sera from highly sensitized multiparous dialysis patients: antibody class, relationship with the HLA and with paternal antigens.

1. Sera from 11 highly sensitized multiparous dialysis patients were studied in order to define the target antigens, antibody class and relationship with paternal HLA class I antigens of the underlying lymphocytotoxic antibodies. All sera contained lymphocytotoxic antibodies to over 70% of a panel of lymphocytes from 24 donors (panel reactivity greater than 70%). 2. Inhibition of cytotoxic activity against paternal lymphocytes by monoclonal antibodies to HLA framework determinants indicated that all 11 sera contained lymphocytotoxic antibodies to paternal class I antigens. In addition, five sera contained lymphocytotoxic antibodies to paternal class II antigens. 3. In order to determine the extent to which lymphocytotoxic antibodies were directed to paternal antigens, the panel reactivity of sera was compared before and after absorption with paternal peripheral blood lymphocytes. Over 50% of panel reactivity was absorbed from eight out of 11 sera, and in three of these 11 over 80% was absorbed. In the majority of patients this change in panel reactivity could be ascribed to binding of lymphocytotoxic antibodies to specific paternal class I antigens. 4. Digestion of sera with dithiothreitol had no significant effect on panel reactivity, indicating that the lymphocytotoxic antibodies were of immunoglobulin G class. 5. No sera reacted with either autologous lymphocytes or K562 cells, indicating an absence of autoantibodies. 6. These studies imply that panel-reactive lymphocytotoxic antibodies in the sera of highly sensitized multiparous patients are those which mediate hyperacute renal allograft rejection. Their development may be related to secondary humoral responses to antigens in blood transfusions from donors who share paternal class I specificities.