Abstract

We report that oral infection with Yersinia pseudotuberculosis (Yptb) results in development of two distinct populations of pathogen-specific CD8 tissue-resident memory T (TRM) cells in the lamina propria (LP). CD103– T cells did not require transforming-growth factor-β (TGF-β) signaling, but were true resident memory cells. Unlike CD103+ CD8 T cells, which were TGF-β-dependent and scattered in the tissue, CD103– T cells clustered with CD4 T cells and CX3CR1+ macrophages and/or dendritic cells around areas of bacterial infection. CXCR3-dependent recruitment to inflamed areas was critical for development of the CD103– population and pathogen clearance. These studies have identified the preferential development of CD103– LP TRM cells in inflammatory microenvironments within the LP and suggest that this subset plays a critical role in controlling infection.

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