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TRPV1阳性神经元在先天免疫中的功能获揭示
作者:小柯机器人 发布时间:2019/8/9 16:44:24

美国匹兹堡大学Daniel H. Kaplan研究组发现皮肤TRPV1阳性神经元可触发保护性先天17型预期免疫。2019年8月9日出版的《细胞》发表了这项成果。

研究人员在没有组织损伤或病原体相关产物的情况下,使用TRPV1-Ai32光遗传小鼠和皮肤光刺激来激活皮肤神经元。研究人员发现TRPV1阳性神经元激活足以引发局部17型免疫应答,从而增强宿主对白色念珠菌和金黄色葡萄球菌的防御。此外,局部神经元激活可以引发17型免疫反应并通过神经反射弧增强邻近未受刺激皮肤的宿主防御。这些数据显示TRPV1阳性神经元能够激活对宿主防御,并证明在依赖于逆行神经元激活的感染邻近位点存在功能性预期先天免疫。

据了解,皮肤的TRPV1阳性神经元直接感知有害刺激、炎性细胞因子和病原体相关分子,并且是对抗某些皮肤病原体的先天免疫所必需的。尚未解决的重要问题是,单独激活TRPV1阳性神经元是否足以启动先天免疫反应,以及TRPV1阳性神经元启动免疫反应的生物学功能是什么。


附:英文原文

Title: Cutaneous TRPV1+ Neurons Trigger Protective Innate Type 17 Anticipatory Immunity

Author: Jonathan A. Cohen, Tara N. Edwards, Andrew W. Liu, Toshiro Hirai, Marsha Ritter Jones, Jianing Wu, Yao Li, Shiqun Zhang, Jonhan Ho, Brian M. Davis, Kathryn M. Albers, Daniel H. Kaplan

Issue&Volume: Volume 178 Issue 4

Abstract: Cutaneous TRPV1 + neurons directly sense noxious stimuli, inflammatory cytokines, and pathogen-associated molecules and are required for innate immunity against some skin pathogens. Important unanswered questions are whether TRPV1 + neuron activation in isolation is sufficient to initiate innate immune responses and what is the biological function for TRPV1 + neuron-initiated immune responses. We used TRPV1-Ai32 optogenetic mice and cutaneous light stimulation to activate cutaneous neurons in the absence of tissue damage or pathogen-associated products. We found that TRPV1 + neuron activation was sufficient to elicit a local type 17 immune response that augmented host defense to C. albicans and S. aureus. Moreover, local neuron activation elicited type 17 responses and augmented host defense at adjacent, unstimulated skin through a nerve reflex arc. These data show the sufficiency of TRPV1 + neuron activation for host defense and demonstrate the existence of functional anticipatory innate immunity at sites adjacent to infection that depends on antidromic neuron activation.

DOI: https://doi.org/10.1016/j.cell.2019.06.022

Source: https://www.cell.com/cell/fulltext/S0092-8674(19)30685-3

期刊信息
Cell:《细胞》,创刊于1974年。隶属于细胞出版社,最新IF:36.216
官方网址:https://www.cell.com/