Abstract
Efficient host defense relies on the ability to mount context-dependent immune responses. Dendritic cells (DCs) sense pathogens and tissue damage and subsequently migrate to lymph nodes to present antigens to naive T cells. Through the production of cytokines, DCs further instruct other immune cells about which type of immune response is needed (1). For example, DC-derived interleukin-23 (IL-23) in the skin promotes efficient defense against Candida albicans and Staphylococcus aureus infections, but it also drives psoriasislike skin inflammation (2, 3). Nociceptors are somatosensory neurons that innervate barrier organs and detect noxious stimuli, including mechanical injury, reactive chemicals, inflammatory mediators, and pathogens (4). Nociceptors relay noxious stimuli to the brain as pain or itching sensation and release neuropeptides, which can influence immune cells (4). On page 1315 of this issue, HanĨ et al. (5) report the identification of multiple mechanisms by which nociceptors can regulate DCs in the skin.
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