Endogenous CD100 promotes glomerular injury and macrophage recruitment in experimental crescentic glomerulonephritis

Endogenous CD100 promotes glomerular injury and macrophage recruitment in experimental crescentic glomerulonephritis. CD100 participates in adaptive immune responses and is important in neural cell migration. To determine the role of endogenous CD100 in severe glomerular inflammation, we induced experimental crescentic glomerulonephritis by planting a foreign antigen in glomeruli of sensitized normal and CD100-deficient (CD100)/)) mice. Fewer CD100)/) glomeruli exhibited crescent formation or severe histological changes. Antigenspecific immune responses were reduced in CD100)/) mice. There was less interferon (IFN)-c and interleukin (IL)-4 production by splenocytes and fewer activated T and B cells were present in lymph nodes of immunized CD100)/) mice.