The expression of HLA class I was assessed on erythrocytes by haemagglutination with monoclonal antibodies to monomorphic epitopes on the heavy and light (ß2-microglobulin) chains. Previously, enhancement of HLA class I expression was observed on erythrocytes of many patients with systemic lupus erythematosus (SLE) and chronic lymphatic leukaemia (CLL), and we have now tested erythrocytes from patients (and 130 normal controls) with other auto-immune diseases and renal and haematological disorders. The striking enhancement in patients with SLE and CLL was confirmed. A significant increase in expression was also observed in aplastic anaemia patients following bone marrow transplantation and in renal patients with primary glomerulonephritis who had received a transplant. No class I was expressed by erythrocytes from many patients with inherited haemoglobinopathies and high reticulocyte counts, which suggests that the enhancement in SLE patients cannot be accounted for by immature or young erythrocyte populations. The distribution of HLA-A and -B types in the patients with enhanced class I expression did not relate to those antigens previously detected more frequently on erythrocytes, B7(Bg(a)), B17(Bg(b)), A28(Bgc), B8 or A10, and the enhancement was not associated with any particular HLA types.

The expression of HLA class I was assessed on erythrocytes by haemagglutination with monoclonal antibodies to monomorphic epitopes on the heavy and light (beta 2-microglobulin) chains. Previously, enhancement of HLA class I expression was observed on erythrocytes of many patients with systemic lupus erythematosus (SLE) and chronic lymphatic leukaemia (CLL), and we have now tested erythrocytes from patients (and 130 normal controls) with other auto-immune diseases and renal and haematological disorders. The striking enhancement in patients with SLE and CLL was confirmed. A significant increase in expression was also observed in aplastic anaemia patients following bone marrow transplantation and in renal patients with primary glomerulonephritis who had received a transplant. No class I was expressed by erythrocytes from many patients with inherited haemoglobinopathies and high reticulocyte counts, which suggests that the enhancement in SLE patients cannot be accounted for by immature or young erythrocyte populations. The distribution of HLA-A and -B types in the patients with enhanced class I expression did not relate to those antigens previously detected more frequently on erythrocytes, B7(Bga), B17(Bgb), A28(Bgc), B8 or A10, and the enhancement was not associated with any particular HLA types.