期刊
NATURE IMMUNOLOGY
卷 13, 期 7, 页码 667-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2319
关键词
-
类别
资金
- US National Institutes of Health [AI19335]
- Howard Hughes Medical Institute
T cell-specific deletion of the receptor for transforming growth factor-beta (TGF-beta) mediated by Cre recombinase expressed early in T cell development leads to early-onset lethal autoimmune disease that cannot be controlled by regulatory T cells. However, when we deleted that receptor through the use of Cre driven by a promoter that is active much later in T cell development, adult mice in which most peripheral CD4(+) or CD8(+) T cells lacked the receptor for TGF-beta showed no signs of autoimmunity. Because of their enhanced responses to weak stimulation of the T cell antigen receptor, when transferred into lymphopenic recipients, naive TGF-beta-unresponsive T cells underwent much more proliferation and differentiation into effector cells and induced lymphoproliferative disease. We propose that TGF-beta signaling controls the self-reactivity of peripheral T cells but that in the absence of TGF-beta signals, an added trigger such as lymphopenia is needed to drive overt autoimmune disease.
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