Intestinal macrophages expressing the fraktalkine receptor (CX3CR1+) 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 CX3CR1+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 CX3CR1-mediated pathogen exclusion is part of a defensive strategy against infections that includes multiple effector mechanisms acting synergistically at the intestinal mucosa.

中文翻译：

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肠CX3CR1 +巨噬细胞的多方面性格

表达Fraktalkine受体（CX3CR1 +）的肠道巨噬细胞代表着一系列细胞，它们的作用范围从保持肠道免疫稳态稳定到通过扩展跨上皮树突（TEDs）捕获腔微生物并将其穿梭于上皮细胞来控制抗原的访问。启动免疫反应。但是，最近的证据表明，在感染的早期，捕获病原体的CX3CR1 +巨噬细胞迁移到小肠的内腔，因此阻止了病原体穿过上皮。