Proinflammatory microenvironments within the intestine regulate the differentiation of tissue-resident CD8+ T cells responding to infection

被引:225
作者
Bergsbaken, Tessa
Bevan, Michael J. [1 ]
机构
[1] Univ Washington, Dept Immunol, Seattle, WA 98195 USA
基金
美国国家卫生研究院;
关键词
CHEMOKINE RECEPTOR CXCR3; YERSINIA-PSEUDOTUBERCULOSIS; PESTIS INFECTION; DENDRITIC CELLS; ORAL INFECTION; EFFECTOR-CELLS; MEMORY; MIGRATION; ANTIGEN; GENERATION;
D O I
10.1038/ni.3108
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
We report that oral infection with Yersinia pseudotuberculosis results in the development of two distinct populations of pathogen-specific CD8(+) tissue-resident memory T cells (T-RM cells) in the lamina propria. CD103(-) T cells did not require transforming growth factor-beta (TGF-beta) signaling but were true resident memory cells. Unlike CD103(+)CD8(+) T cells, which were TGF-beta dependent and were scattered in the tissue, CD103(-)CD8(+) T cells clustered with CD4(+) T cells and CX3CR1(+) macrophages and/or dendritic cells around areas of bacterial infection. CXCR3-dependent recruitment of cells to inflamed areas was critical for development of the CD103(-) population and pathogen clearance. Our studies have identified the 'preferential' development of CD103(-) T-RM cells in inflammatory microenvironments within the lamina propria and suggest that this subset has a critical role in controlling infection.
引用
收藏
页码:406 / 414
页数:9
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