期刊
IMMUNITY
卷 49, 期 6, 页码 1049-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2018.10.008
关键词
-
类别
资金
- NIH [AI029564, CA156330, DK094779, CA10068, U19AI109965]
- Japanese vaccine research fellowship (Japan Foundation for Pediatric Research)
Appropriate immune responses require a fine balance between immune activation and attenuation. NLRC3, a non-inflammasome-forming member of the NLR innate immune receptor family, attenuates inflammation in myeloid cells and proliferation in epithelial cells. T lymphocytes express the highest amounts of Nlrc3 transcript where its physiologic relevance is unknown. We show that NLRC3 attenuated interferon-gamma and TNF expression by CD4(+) T cells and reduced T helper 1 (Th1) and Th17 cell proliferation. Nlrc3(-/-) mice exhibited increased and prolonged CD4(+) T cell responses to lymphocytic choriomeningitis virus infection andworsened experimental autoimmune encephalomyelitis (EAE). These functions of NLRC3 were executed in a T-cell-intrinsic fashion: NLRC3 reduced K63-linked ubiquitination of TNF-receptor-associated factor 6 (TRAF6) to limit NF-kappa B activation, lowered phosphorylation of eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), and diminished glycolysis and oxidative phosphorylation. This study reveals an unappreciated role for NLRC3 in attenuating CD4(+) T cell signaling and metabolism.
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