Jill Roberts Institute for Research in IBD, Division of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, New York, USA.
Gut Microbes. 2020;11(2):231-236. doi: 10.1080/19490976.2019.1638725. Epub 2019 Jul 26.
Despite continuous exposure to trillions of microbes, the intestinal immune system protects the mucosa by balancing barrier protection, tolerance, and immunity. As both sentinel and effector, the mucosal innate immune system plays a central role in coordinating these responses. By integrating signals from the intestinal microbiota, mononuclear phagocytes (MNPs) serve as a critical link in regulating effector functions of group 3 innate lymphoid cells (ILC3s). Our recent work identified the role for MNP production of the IBD-linked protein TNF-like ligand 1A (TL1A) in modulating microbial regulation of ILC3 barrier immunity. These findings highlight a broader role for ILC3s in local control of T cell immunity and their potential role in the pathogenesis and treatment of inflammatory disease.
尽管不断接触到万亿计的微生物,肠道免疫系统通过平衡屏障保护、耐受和免疫来保护黏膜。作为哨点和效应器,黏膜固有免疫系统在协调这些反应中起着核心作用。单核吞噬细胞(MNPs)通过整合来自肠道微生物群的信号,作为调节 3 组固有淋巴细胞(ILC3)效应功能的关键环节。我们最近的工作确定了 MNPs 产生与 IBD 相关的蛋白 TNF 样配体 1A(TL1A)在调节 ILC3 屏障免疫中的微生物调节作用。这些发现强调了 ILC3 在局部控制 T 细胞免疫中的更广泛作用及其在炎症性疾病发病机制和治疗中的潜在作用。