Anti-IgM treatment of C57BL/6-1pr/1pr mice: depletion of B cells reduces 1pr gene-induced lymphoproliferation and mononuclear cell vasculitis.
In order to study the role of B cells in autoimmune abnormalities observed in C57BL/6 mice bearing the autosomal mutant gene 1pr (lymphoproliferation), we treated mice from birth continuously with rabbit anti-IgM antiserum. Anti-IgM treatment resulted in the complete suppression of B cell development, documented by the absence of surface Ig-positive cells, the lack of lipopolysacchride-induced mitogenic responses, and the lack of autoantibody production. Although, anti-IgM-treated C57BL/6-1pr/1pr mice developed 1pr gene-associated lymphoproliferation due to the accumulation of Thy-1+, CD4-, CD8-, B220+ T lymphocytes in spleen and lymph nodes, the size of their spleen and lymph nodes was considerably smaller than that of normal rabbit serum-treated C57BL/6-1pr/1pr mice. Systemic vascular lesions associated with mononuclear cell infiltration were a little affected by anti-IgM treatment. This indicates that the development of mononuclear cell vasculitis in mice bearing the 1pr gene may be associated with the 1pr gene-induced lymphoproliferation and is independent of B cells and autoantibody production.
Cerny
A
A
Department of Pathology, University of Geneva, Switzerland.
Kimoto
M
M
Hügin
A W
AW
Merino
R
R
Izui
S
S
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis; D001327:Autoimmune Diseases / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D007075:Immunoglobulin M / Q000276:immunology; D008213:Lymphocyte Activation; D008212:Lymphocyte Depletion; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009154:Mutation; D014657:Vasculitis / Q000276:immunology*
D000888:Antibodies, Anti-Idiotypic; D001323:Autoantibodies; D007075:Immunoglobulin M