生物
免疫学
炎症
CD8型
促炎细胞因子
细胞生物学
人口
细胞分化
免疫系统
医学
遗传学
环境卫生
基因
作者
Tessa Bergsbaken,Michael J. Bevan,Pamela J. Fink
出处
期刊:Cell Reports
[Elsevier]
日期:2017-04-01
卷期号:19 (1): 114-124
被引量:119
标识
DOI:10.1016/j.celrep.2017.03.031
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI