Interleukin-7 is required for CD4(+) T cell activation and autoimmune neuroinflammation.

Abstract IL-7 is known to be vital for T cell homeostasis but has previously been presumed to be dispensable for TCR-induced activation. Here, we show that IL-7 is critical for the initial activation of CD4 + T cells in that it provides some of the necessary early signaling components, such as activated STAT5 and Akt. Accordingly, short-term in vivo IL-7Rα blockade inhibited the activation and expansion of autoantigen-specific CD4 + T cells and, when used to treat experimental autoimmune encephalomyelitis (EAE), prevented and ameliorated disease. Our studies demonstrate that IL-7 signaling is a prerequisite for optimal CD4 + T cell activation and that IL-7R antagonism may be effective in treating CD4 + T cell-mediated neuroinflammation and other autoimmune inflammatory conditions.