[C-type murine leukemia virus and the pathogenesis of necrotizing arteritis and glomerulonephritis in MRL/1 mice].

A comparative immunopathological and electron microscopic study of vasculitis and glomerulonephritis in autoimmune mice (B/W F1, SL/Ni, MRL/1) was performed. The pathogenesis of vasculitis in B/W F1 mice is due to the deposition of circulating murine leukemia virus (MuLV) gp70-immune complexes in the subendothelial space of vascular walls. Whereas, the vasculitis in SL/Ni mice is mediated by the budding of MuLV particles from vascular smooth muscle cells and the humoral immune response (Gross natural antibody) to virions and MuLV related cell surface antigens of vascular smooth muscle cells. The vasculitis in MRL/1 mice seems to be mediated mainly by the deposition of gp 70-immune complexes in vascular walls. However, the perivascular infiltration of thy1 . 2 antigen positive T-lymphocytes in an early stage of vasculitis suggests that the cellular immune response is, at least in part, important for the initiation of vasculitis in MRL/1 mice. The collective evidence suggests that several immunologic mechanisms are at works in the production of naturally occurring vasculitides in B/W F1, SL/Ni, and MRL/1 mice. The common pathogenesis of glomerulonephritis in B/W F1, SL/Ni and MRL/1 mice is the deposition of circulating gp70-immune complexes in the glomeruli. In addition, in the case of SL/Ni mice, glomerulonephritis is in some part initiated by local formations of the immune complex in the mesangium. The occurrence of vasculitis in MRL/1 mice is markedly accelerated by the treatment of methoxamine hydrochloride (Mexan), as was shown previously in SL/Ni mice.