A role for Stat5 in CD8+ T cell homeostasis
A role for Stat5 in CD8+ T cell homeostasis
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DOI：
10.4049/jimmunol.170.1.210
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发表时间：
2003-01-01
影响因子：
4.4
通讯作者：
Leonard, WJ
中科院分区：
文献类型：
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作者：
Kelly, J;Spolski, R;Leonard, WJ
细胞因子信号已知有助于CD8(+)记忆性T细胞的内稳态，但对其机制的确切理解一直难以捉摸。我们现在已经研究了Stat5蛋白在这一过程中的作用。Stat5a和Stat5b基因敲除小鼠的CD8(+) T细胞数量减少，而Stat5转基因小鼠的这些细胞数量增加。Stat5b转基因小鼠表现出抗原诱导的CD4(+) T细胞死亡增加，以及CD8(+) T细胞增殖和Bcl - 2表达增强，为这一发现提供了依据。此外，CD8(+)记忆性T细胞受到Stat5水平的显著影响。这些发现确定Stat5蛋白是细胞因子用于调节CD8(+) T细胞内稳态的关键信号传导介质。
Cytokine signals are known to contribute to CD8(+) memory T cell homeostasis, but an exact understanding of the mechanism(s) has remained elusive. We have now investigated the role of Stat5 proteins in this process. Whereas Stat5a and Stat5b KO mice have decreased numbers of CD8(+) T cells, Stat5-transgenic mice have an increased number of these cells. Stat5b-transgenic mice exhibit increased Ag-induced cell death of CD4(+) T cells and augmented proliferation and Bcl-2 expression in CD8(+) T cells, providing a basis for this finding. Moreover, CD8(+) memory T cells are substantially affected by Stat5 levels. These findings identify Stat5 proteins as critical signaling mediators used by cytokines to regulate CD8(+) T cell homeostasis.