Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy.
Department of Experimental and Clinical Medicine, Section of Anatomy, University of Florence, Florence, Italy.
Trends Immunol. 2017 Dec;38(12):879-887. doi: 10.1016/j.it.2017.07.009. Epub 2017 Aug 24.
Intestinal macrophages expressing the fraktalkine receptor (CXCR1) represent a cell population that plays a variety of roles ranging from maintaining intestinal immune homeostasis at steady state to controlling antigen access by extending transepithelial dendrites (TEDs) to capture luminal microbes and shuttle them across the epithelium to initiate immune responses. However, recent evidence shows that very early during infection, pathogen-capturing CXCR1 macrophages migrate to the lumen of the small intestine, therefore preventing pathogens from traversing the epithelium. Here we discuss the complexity of the at-times seemingly opposing roles played by these cells and propose that CXCR1-mediated pathogen exclusion is part of a defensive strategy against infections that includes multiple effector mechanisms acting synergistically at the intestinal mucosa.
表达趋化因子（ fractalkine ）受体（ CXCR1 ）的肠道巨噬细胞代表了一类发挥多种作用的细胞群体，这些作用从在稳态下维持肠道免疫平衡，到通过延伸跨上皮树突（ TEDs ）来控制抗原进入，以捕获腔微生物并将其穿过上皮细胞运送到启动免疫反应。然而，最近的证据表明，在感染的早期，捕获病原体的 CXCR1 巨噬细胞迁移到小肠的腔中，从而防止病原体穿过上皮细胞。在这里，我们讨论了这些细胞有时似乎相互矛盾的作用的复杂性，并提出了 CXCR1 介导的病原体排斥是针对感染的防御策略的一部分，该策略包括在肠道黏膜上协同作用的多种效应机制。
