作者
Xin Chen, Ryoko Hamano, Jeffrey J Subleski, Arthur A Hurwitz, OM Howard, Joost J Oppenheim
发表日期
2010/7/1
期刊
The Journal of Immunology
卷号
185
期号
1
页码范围
174-182
出版商
American Association of Immunologists
简介
Our previous study showed that TNFR2 is preferentially expressed by CD4+ FoxP3+ regulatory T cells (Tregs), and expression of this receptor identified maximally suppressive Tregs. TNFR2 is also expressed by a small fraction of CD4+ FoxP3− conventional T cells (Tconvs) in normal mice, and its expression is upregulated by T cell activation. This raises questions about the role of TNFR2 signaling in the function of Tconv cells. In this study, by using FoxP3/gfp knock-in mice, we showed that TNFR2 signaling did not induce FoxP3− CD4 cells to become suppressive. Ki-67, a marker of proliferation, was concomitantly expressed with TNFR2 by CD4 cells, independent of forkhead box P3 expression, in normal mice and Lewis lung carcinoma-bearing mice. TNFR2 is associated with greater suppressive functions when expressed by Tregs and is associated with greater resistance to suppression when expressed by …
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