期刊
JOURNAL OF IMMUNOLOGY
卷 206, 期 11, 页码 2725-2739出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2000647
关键词
-
类别
资金
- U.K. Research and Innovation Medical Research Council [MR/M003493/1]
- British Heart Foundation [PG/12/36/29444]
- U.K. National Institute for Health Research Comprehensive Biomedical Research Centre
- King's College London
- King's College Hospital National Health Service Foundation Trust
- Marie Sklodowska-Curie Fellowship
- King's Prize fellowship
miR-142 plays a critical role in the homeostasis and function of ILC2s, deficiency of miR-142 leads to biased development of ILC2 progenitors and significant changes in phenotype, affecting ILC2-mediated immune responses.
Innate lymphoid cells are central to the regulation of immunity at mucosal barrier sites, with group 2 innate lymphoid cells (ILC2s) being particularly important in type 2 immunity. In this study, we demonstrate that microRNA(miR)-142 plays a critical, cell-intrinsic role in the homeostasis and function of ILC2s. Mice deficient for miR-142 expression demonstrate an ILC2 progenitor-biased development in the bone marrow, and along with peripheral ILC2s at mucosal sites, these cells display a greatly altered phenotype based on surface marker expression. ILC2 proliferative and effector functions are severely dysfunctional following Nippostrongylus brasiliensis infection, revealing a critical role for miR-142 isoforms in ILC2-mediated immune responses. Mechanistically, Socs1 and Gfi1 expression are regulated by miR-142 isoforms in ILC2s, impacting ILC2 phenotypes as well as the proliferative and effector capacity of these cells. The identification of these novel pathways opens potential new avenues to modulate ILC2-dependent immune functions.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据