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However, the signal determining how activated microglia affects the fate of neuronal cells remains largely unknown. Here we demonstrate that DNAX\u2010activating protein of 12 kDa (DAP12), a transmembrane adaptor protein that contains an immunoreceptor tyrosine\u2010based activation motif, is a critical regulator of microglial function after nerve injury. In a model of mouse hypoglossal nerve injury, the duration of microglial increase after nerve injury became shorter in mice lacking\n                    <jats:italic>DAP12<\/jats:italic>\n                    , although microglial morphology and total cell numbers were not significantly affected during early phase after nerve injury. Intriguingly, expressions of M1\u2010phenotype markers including pro\u2010inflammatory cytokines were suppressed in\n                    <jats:italic>DAP12<\/jats:italic>\n                    \u2010deficient microglia. Furthermore, axotomy\u2010induced motor neuron death was markedly prevented in\n                    <jats:italic>DAP12<\/jats:italic>\n                    \u2010deficient mice. Collectively, DAP12\u2010mediated microglial activation following axotomy promotes pro\u2010inflammatory responses, and thereby accelerates nerve injury\u2010induced neuron death, suggesting that DAP12 is a potential therapeutic target for the protection of neuronal degeneration caused by microglial activation. 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