Rochman Yrina, Leonard Warren J
Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD20892-1674, USA.
J Immunol. 2008 Dec 1;181(11):7699-705. doi: 10.4049/jimmunol.181.11.7699.
Thymic stromal lymphopoietin (TSLP) is a cytokine produced by stromal cells, epithelial cells, and basophils that acts on dendritic cells, mast cells, and CD4(+) T cells. The receptor for TSLP contains a TSLP-specific receptor chain (TSLPR) and the IL-7R alpha-chain. Although IL-7 critically controls the expansion and survival of naive and memory CD8(+) T cells, an action for TSLP on CD8(+) T cells has not been reported. We now demonstrate that CD8(+) T cells express TSLPR and that TSLP activates both STAT5 and Akt and induces Bcl-2 in these cells. Correspondingly, TSLP increases CD8(+) T cell survival in vitro as well as in wild-type and T-depleted mice in vivo, without altering the homeostatic proliferation of these cells. Moreover, TSLP can maintain CD8(+) T cells even in the absence of IL-7. Thus, our data reveal that TSLP contributes to CD8(+) T cell homeostasis in both normal and lymphopenic conditions.
胸腺基质淋巴细胞生成素(TSLP)是一种由基质细胞、上皮细胞和嗜碱性粒细胞产生的细胞因子,作用于树突状细胞、肥大细胞和CD4(+) T细胞。TSLP的受体包含一个TSLP特异性受体链(TSLPR)和IL-7Rα链。尽管IL-7对初始和记忆性CD8(+) T细胞的扩增和存活至关重要,但尚未有关于TSLP对CD8(+) T细胞作用的报道。我们现在证明CD8(+) T细胞表达TSLPR,并且TSLP能激活这些细胞中的STAT5和Akt,并诱导Bcl-2表达。相应地,TSLP在体外以及在野生型和T细胞耗竭的小鼠体内均能提高CD8(+) T细胞的存活率,而不改变这些细胞的稳态增殖。此外,即使在没有IL-7的情况下,TSLP也能维持CD8(+) T细胞。因此,我们的数据表明TSLP在正常和淋巴细胞减少的情况下均有助于CD8(+) T细胞的稳态。