期刊
JOURNAL OF IMMUNOLOGY
卷 183, 期 7, 页码 4493-4501出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0804339
关键词
-
类别
资金
- NIAID NIH HHS [R01 AI037584-11A1, R01 AI037584-12, R01 AI037584-15, R01 AI046564-07, R01 AI046564-06A2, R01 AI037584-13, R01 AI046564, R01 AI084987, AI46564, R01 AI046564-09, R01 AI037584, R01 AI046564-08, R01 AI037584-14, AI37584] Funding Source: Medline
- NIDDK NIH HHS [P30 DK032520, DK32520] Funding Source: Medline
T cell proliferation following activation is an essential aspect of the adaptive immune response. Multiple factors, such as TCR signaling, costimulation, and signals from cytokines, each contribute to determine the magnitude of T cell expansion. In this report, we examine in detail the role of Jak3/common -gamma-chain-dependent cytokines in promoting cell cycle progression and proliferation of naive T cells. Using naive CD4(+) T cells from Jak3-deficient mice and wild-type CD4(+) T cells treated with a small molecule inhibitor of Jak3, we find that these cytokine signals are not required for proliferation; instead, they are important for the survival of activated T cells. In addition, we show that the percentage of cells entering the cell cycle and the percentage of cells in each round of cell division are comparable between Jak3-deficent and wild-type T cells. Furthermore, cell cycle progression and the regulated expression of key cell cycle proteins are independent of Jak3/common gamma-chain cytokine signals. These findings hold true over a wide range of TCR signal strengths. However, when CD28 costimulatory signals, but not TCR signals, are limiting, Jak3-dependent cytokine signals become necessary for the proliferation of naive T cells. Because CD28 signaling has been found to be dispensable for autoreactive T cell responses, these data suggest the potential for interfering with autoimmune T cell responses by inhibition of Jak3 signaling. The Journal of Immunology, 2009, 183: 4493-4501.
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