期刊
NATURE IMMUNOLOGY
卷 16, 期 4, 页码 406-414出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3108
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资金
- Howard Hughes Medical Institute
- US National Institutes of Health [AI-19335]
- Cancer Research Institute
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R37AI019335, R01AI019335] Funding Source: NIH RePORTER
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.
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