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白细胞介素-10 受体信号在先天免疫细胞中调节黏膜免疫耐受和抗炎性巨噬细胞功能。

Interleukin-10 receptor signaling in innate immune cells regulates mucosal immune tolerance and anti-inflammatory macrophage function.

机构信息

Division of Gastroenterology, Hepatology and Nutrition, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; interNational Early Onset Paediatric IBD Cohort Study (NEOPICS).

Division of Gastroenterology, Hepatology and Nutrition, Boston Children's Hospital, Boston, MA 02115, USA; interNational Early Onset Paediatric IBD Cohort Study (NEOPICS).

出版信息

Immunity. 2014 May 15;40(5):706-19. doi: 10.1016/j.immuni.2014.03.011. Epub 2014 May 1.

DOI:10.1016/j.immuni.2014.03.011
PMID:24792912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4513358/
Abstract

Intact interleukin-10 receptor (IL-10R) signaling on effector and T regulatory (Treg) cells are each independently required to maintain immune tolerance. Here we show that IL-10 sensing by innate immune cells, independent of its effects on T cells, was critical for regulating mucosal homeostasis. Following wild-type (WT) CD4(+) T cell transfer, Rag2(-/-)Il10rb(-/-) mice developed severe colitis in association with profound defects in generation and function of Treg cells. Moreover, loss of IL-10R signaling impaired the generation and function of anti-inflammatory intestinal and bone-marrow-derived macrophages and their ability to secrete IL-10. Importantly, transfer of WT but not Il10rb(-/-) anti-inflammatory macrophages ameliorated colitis induction by WT CD4(+) T cells in Rag2(-/-)Il10rb(-/-) mice. Similar alterations in the generation and function of anti-inflammatory macrophages were observed in IL-10R-deficient patients with very early onset inflammatory bowel disease. Collectively, our studies define innate immune IL-10R signaling as a key factor regulating mucosal immune homeostasis in mice and humans.

摘要

完整的白细胞介素-10 受体（IL-10R）信号在效应器和 T 调节（Treg）细胞上的信号传递，各自独立地维持着免疫耐受。在这里，我们发现先天免疫细胞对 IL-10 的感应，独立于其对 T 细胞的作用，对于调节黏膜稳态至关重要。在野生型（WT）CD4(+)T 细胞转移后，Rag2(-/-)Il10rb(-/-)小鼠发展为严重的结肠炎，同时 Treg 细胞的生成和功能也出现严重缺陷。此外，IL-10R 信号的缺失损害了抗炎性肠道和骨髓来源的巨噬细胞的生成和功能，以及它们分泌 IL-10 的能力。重要的是，WT 而非 Il10rb(-/-)抗炎性巨噬细胞的转移，改善了 Rag2(-/-)Il10rb(-/-)小鼠中 WT CD4(+)T 细胞诱导的结肠炎。在具有非常早发性炎症性肠病的 IL-10R 缺陷患者中，也观察到抗炎性巨噬细胞的生成和功能出现类似的改变。总的来说，我们的研究定义了先天免疫 IL-10R 信号作为调节小鼠和人类黏膜免疫稳态的关键因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7812/4513358/51257cbc0b92/nihms-592739-f0007.jpg
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