Nociceptive Sensory Fibers Drive Interleukin-23 Production from CD301b+ Dermal Dendritic Cells and Drive Protective Cutaneous Immunity.
Nociceptive Sensory Fibers Drive Interleukin-23 Production from CD301b+ Dermal Dendritic Cells and Drive Protective Cutaneous Immunity.
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DOI：
10.1016/j.immuni.2015.08.016
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发表时间：
2015-09-15
期刊：
影响因子：
32.4
通讯作者：
Kaplan DH
中科院分区：
文献类型：
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作者：
Kashem SW;Riedl MS;Yao C;Honda CN;Vulchanova L;Kaplan DH
粘膜组织中对白色念珠菌的先天性抵抗需要在感染早期由组织驻留细胞产生白细胞介素-17A（IL-17 A），但细胞因子产生的机制尚未精确定义。在皮肤中，我们发现真皮γδ T细胞是C.白色念珠菌感染，并需要病原体抗性。从真皮γδ T细胞诱导IL-17 A和对C.白念珠菌需要从CD 301 b+真皮树突状细胞（dDC）产生IL-23。此外，我们还发现C.白色念珠菌感觉神经元的消融增加了对C.白色念珠菌感染，这可以通过外源性添加神经肽CGRP来挽救。这些数据定义了一种模型，其中皮肤中的伤害感受途径驱动CD 301 b + dDC产生IL-23，导致γδ T细胞产生IL-17 A并对皮肤念珠菌病产生抗性。
Innate resistance to Candida albicans in mucosal tissues requires the production of interleukin-17A (IL-17A) by tissue-resident cells early during infection, but the mechanism of cytokine production has not been precisely defined. In the skin, we found that dermal γδ T cells were the dominant source of IL-17A during C. albicans infection and were required for pathogen resistance. Induction of IL-17A from dermal γδ T cells and resistance to C. albicans required IL-23 production from CD301b+ dermal den-dritic cells (dDCs). In addition, we found that sensory neurons were directly activated by C. albicans. Ablation of sensory neurons increased susceptibility to C. albicans infection, which could be rescued by exogenous addition of the neuropeptide CGRP. These data define a model in which nociceptive pathways in the skin drive production of IL-23 by CD301b+ dDCs resulting in IL-17A production from γδ T cells and resistance to cutaneous candidiasis.