CD4 positive T cells directly associate with development of lupus nephritis.

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Lupus-prone MRL/lpr mice, that lack interferon regulatory factor 4 (Irf4-/-MRL/lpr), develop cellular proliferative glomerulonephritis with significantly increased numbers of splenic CD4+ T cells, despite lack of antibody production and immune complex (IC) formation. To investigate the underlying mechanisms of the development of nephritis in these mice, CD4+ T cells proliferating in their spleen were analyzed. Compared to controls, Irf4-/-MRL/lpr had significantly increased numbers of IFN-γ producing Th1-type cells, and significantly increased numbers of CD62L+/CD44+ memory CD4+ T cells and CD62L-/CD44+ effector CD4+ T cells. Similar results were observed in Irf4-/-NZM2410 mice, another murine lupus model. These results suggest that Irf4 associate with the development of IFN-γ producing memory and effector Th1 cells, and the association of these cells with the development of non-IC-dependent lupus-like glomerulonephritis observed in Irf4-deficient murine models of human SLE.