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.