Kim Myunghoo, Hill Andrea A, Wu Wan-Jung, Diehl Gretchen E
Alkek Center for Metagenomics and Microbiome Research and the Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA.
Department of Animal Science, Pusan National University, Busan, Republic of Korea.
Gut Microbes. 2019 Jul 4;10(4):540-546. doi: 10.1080/19490976.2018.1559683. Epub 2019 Jan 6.
Intestinal damage driven by unrestricted immune responses against the intestinal microbiota can lead to the development of inflammatory diseases including inflammatory bowel disease. How such breakdown in tolerance occurs alongside the mechanisms to reinforce homeostasis with the microbiota are a focus of many studies. Our recent work demonstrates coordinated interactions between intact microbiota and CXCR1 expressing intestinal antigen presenting cells (APCs) that limits T helper 1 cell responses and promotes differentiation of regulatory T cells (Treg) against intestinal antigens including pathogens, soluble proteins and the microbiota itself. We find a microbial attachment to intestinal epithelial cells is necessary to support these anti-inflammatory immune functions. In this addendum, we discuss how our findings enhance understanding of microbiota-directed homeostatic functions of the intestinal immune system and implications of modulating this interaction in ameliorating inflammatory disease.
针对肠道微生物群的不受限制的免疫反应所驱动的肠道损伤可导致包括炎症性肠病在内的炎症性疾病的发展。这种耐受性的破坏是如何与增强与微生物群的稳态机制同时发生的，是许多研究的重点。我们最近的工作表明，完整的微生物群与表达CXCR1的肠道抗原呈递细胞（APC）之间存在协调的相互作用，这种相互作用限制了辅助性T细胞1型反应，并促进了针对包括病原体、可溶性蛋白质和微生物群本身在内的肠道抗原的调节性T细胞（Treg）的分化。我们发现微生物附着于肠道上皮细胞对于支持这些抗炎免疫功能是必要的。在本附录中，我们讨论了我们的发现如何增进对肠道免疫系统微生物群导向的稳态功能的理解，以及调节这种相互作用在改善炎症性疾病中的意义。
