TLR5 信号刺激 CD3(neg)CD127+免疫细胞在脾脏和黏膜中先天产生 IL-17 和 IL-22。
TLR5 signaling stimulates the innate production of IL-17 and IL-22 by CD3(neg)CD127+ immune cells in spleen and mucosa.
机构信息
Institut Pasteur de Lille, Centre d'Infection et d'Immunité de Lille, France.
出版信息
J Immunol. 2010 Jul 15;185(2):1177-85. doi: 10.4049/jimmunol.1000115. Epub 2010 Jun 21.
Abstract
In adaptive immunity, Th17 lymphocytes produce the IL-17 and IL-22 cytokines that stimulate mucosal antimicrobial defenses and tissue repair. In this study, we observed that the TLR5 agonist flagellin induced swift and transient transcription of genes encoding IL-17 and IL-22 in lymphoid, gut, and lung tissues. This innate response also temporarily enhanced the expression of genes associated with the antimicrobial Th17 signature. The source of the Th17-related cytokines was identified as novel populations of CD3(neg)CD127(+) immune cells among which CD4-expressing cells resembling lymphoid tissue inducer cells. We also demonstrated that dendritic cells are essential for expression of Th17-related cytokines and so for stimulation of innate cells. These data define that TLR-induced activation of CD3(neg)CD127(+) cells and production of Th17-related cytokines may be crucial for the early defenses against pathogen invasion of host tissues.
摘要
在适应性免疫中，Th17 淋巴细胞产生白细胞介素 17（IL-17）和白细胞介素 22（IL-22）细胞因子，刺激黏膜抗菌防御和组织修复。在这项研究中，我们观察到 TLR5 激动剂鞭毛蛋白诱导淋巴组织、肠道和肺部组织中编码 IL-17 和 IL-22 的基因迅速而短暂的转录。这种先天反应还暂时增强了与抗菌 Th17 特征相关的基因的表达。Th17 相关细胞因子的来源被确定为 CD3(neg)CD127(+)免疫细胞中的新型群体，其中表达 CD4 的细胞类似于淋巴组织诱导细胞。我们还证明树突状细胞对于 Th17 相关细胞因子的表达以及先天细胞的刺激是必不可少的。这些数据定义了 TLR 诱导的 CD3(neg)CD127(+)细胞的激活和 Th17 相关细胞因子的产生可能对宿主组织对抗病原体入侵的早期防御至关重要。
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