Dear Editor, Neural-immune interaction in health and disease is a hot topic in current biomedical research [1,2].While the central nervous system (CNS) regulates systemic immune responses through hormonal and neuronal route,the peripheral nervous system (PNS) appears to modulate local innate immune responses [1].Our organs are heavily innervated by the peripheral nerves,yet,it is not fully understood how the PNS controls immunity [2].Toll-like receptors (TLRs) are traditionally expressed in immune cells to regulate innate immunity,but recent studies indicated that TLRs (such as TLR3,4 and 7) are also expressed in primary sensory neurons,especially nociceptive neurons in dorsal root ganglia (DRGs)and trigeminal ganglia of the PNS to regulate sensory functions such as pain and itch [3-6].TLR signaling is largely mediated by the myeloid differentiation factor 88(MyD88) protein (but see [7]),and activation of MyD88 in turn activates the NF-κB and MAP kinase pathways,leading to the production of inflammatory cytokines and chemokines for the initiation of innate immunity [3].Increasing evidence suggests that nociceptor neurons play a critical role in host defense and inflammation [8,9].However,the key signaling molecules in nociceptors for the regulation of immunity remain to be identified.To this end,we generated MyD88-conditional knockout (CKO) mice by deleting MyD88 in nociceptive neurons expressing the sodium channel subunit Navl.8 [8,9].
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