Increased immunoglobulin response to gamma-interferon by lymphocytes from patients with systemic lupus erythematosus.
The factors responsible for abnormal B-cell activation in systemic lupus erythematosus (SLE) are incompletely understood. This study tested the hypothesis that the abnormal B-cell activation observed in human SLE may be due to an augmented response to a helper signal. We demonstrated that non-T cells from 10 of 19 SLE patients increased IgG production in response to interferon-gamma (IFN-gamma) by a mean factor of 20.9 +/- 3.9 over resting levels, while controls stimulated a mean factor of 3.0 +/- 0.5 (P less than 0.005). We found no relationship of IFN-gamma responsiveness to disease activity. Serotyping for HLA A, B, C, and D loci suggested that the hyperresponsiveness may be genetically linked to HLA-Cw7. We conclude that IFN-gamma may contribute to the development and perpetuation of SLE in a subset of patients with SLE.
D000917:Antibody Formation / Q000187:drug effects*; D001402:B-Lymphocytes / Q000276:immunology*; D006680:HLA Antigens / Q000032:analysis; D015236:HLA-C Antigens; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation; D011994:Recombinant Proteins / Q000494:pharmacology; D013268:Stimulation, Chemical
D006680:HLA Antigens; D015236:HLA-C Antigens; C040178:HLA-C*70 antigen; D011994:Recombinant Proteins; D007371:Interferon-gamma