Suppression of transferred BXSB male SLE disease by female spleen cells.
The severe autoimmune disease from which BXSB males die at an early age (young) can be transferred into lethally irradiated female recipients by inoculating them with male spleen or bone marrow cells; similar recipients of female spleen or bone marrow cells develop the late-life disease typical of BXSB females. Using this syngeneic cell transfer model, we investigated the possible ability of female splenic and bone marrow cells to modulate the transferred male disease. We found that female spleen cells or the T-enriched subpopulation of such cells successfully retarded the transferred male disease, as observed by the decreased and delayed glomerulonephritis-associated mortality and lowered levels of serum IgG, autoantibodies, and immune complexes. Transfers of female bone marrow or thymus or female splenic T-depleted subpopulations were incapable of suppressing the accelerated male disease. These results indicate that abnormalities of the male spleen or bone marrow inocula responsible for the transferred early autoimmune disease can be modified by female spleen cells, in particular the female T cell component.
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology / Q000637:transplantation; D001854:Bone Marrow Cells; D005260:Female; D005921:Glomerulonephritis / Q000235:genetics / Q000401:mortality / Q000473:pathology; D007165:Immunosuppression Therapy; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology*; D017710:Lymphocyte Transfusion; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains / Q000276:immunology*; D011828:Radiation Chimera; D012737:Sex Factors; D013154:Spleen / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology / Q000637:transplantation; D013950:Thymus Gland / Q000166:cytology