Format

Send to

Choose Destination
Cell Rep. 2017 Apr 4;19(1):114-124. doi: 10.1016/j.celrep.2017.03.031.

Local Inflammatory Cues Regulate Differentiation and Persistence of CD8+ Tissue-Resident Memory T Cells.

Author information

1
Department of Immunology, University of Washington, Seattle, WA 98109, USA. Electronic address: t.bergsbaken@rutgers.edu.
2
Department of Immunology, University of Washington, Seattle, WA 98109, USA.
3
Department of Immunology, University of Washington, Seattle, WA 98109, USA. Electronic address: pfink@uw.edu.

Abstract

Many pathogens initiate infection at mucosal surfaces, and tissue-resident memory T (Trm) cells play an important role in protective immunity, yet the tissue-specific signals that regulate Trm differentiation are poorly defined. During Yersinia infection, CD8+ T cell recruitment to areas of inflammation within the intestine is required for differentiation of the CD103-CD69+ Trm subset. Intestinal proinflammatory microenvironments have elevated interferon (IFN)-β and interleukin-12 (IL-12), which regulated Trm markers, including CD103. Type I interferon-receptor- or IL-12-receptor-deficient T cells functioned similarly to wild-type (WT) cells during infection; however, the inability of T cells to respond to inflammation resulted in defective differentiation of CD103-CD69+ Trm cells and reduced Trm persistence. Intestinal macrophages were the main producers of IFN-β and IL-12 during infection, and deletion of CCR2+ IL-12-producing cells reduced the size of the CD103- Trm population. These data indicate that intestinal inflammation drives phenotypic diversity and abundance of Trm cells for optimal tissue-specific immunity.

KEYWORDS:

CD103; IL-12; bacterial infection; tissue-resident memory T cells

PMID:
28380351
PMCID:
PMC5444811
DOI:
10.1016/j.celrep.2017.03.031
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center