Abstract
Abstract MPYS, a.k.a. STING and MITA, is a newly described signaling adaptor that functions in both innate and adaptive immunity. MPYS transduces apoptotic death signals when aggregated on the B cell surface, but also plays an obligate role in the intracellular sensing of B-DNA and infectious agents. The basis of MPYS signal transduction is unclear. We report that MPYS signals by two distinct pathways. It associates via its juxtamembrane Box 1 and phosphotyrosine motifs with Tyk2 and STAT1, and utilizes these effectors in ISRE activation. Activation of IFNbeta occurs via MPYS association with and activation of TBK1 and IRF3, and is independent of VISA. MPYS (but not VISA) activation of IFNbeta expression is sensitive to LPS-induced TLR4-independent inhibition, but is positively cooperative with TLR signals. Thus MPYS activates multiple, uniquely regulated signaling pathways to mediate resistance to infection and regulation of adaptive immunity.
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