| First Author | Bergsbaken T | Year | 2017 |
| Journal | Cell Rep | Volume | 19 |
| Issue | 1 | Pages | 114-124 |
| PubMed ID | 28380351 | Mgi Jnum | J:254020 |
| Mgi Id | MGI:6103450 | Doi | 10.1016/j.celrep.2017.03.031 |
| Citation | Bergsbaken T, et al. (2017) Local Inflammatory Cues Regulate Differentiation and Persistence of CD8(+) Tissue-Resident Memory T Cells. Cell Rep 19(1):114-124 |
| abstractText | 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)-beta 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-beta 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. |
