由白细胞介素-4诱导的生长因子独立-1调节辅助性T细胞2的增殖。

Growth factor independent-1 induced by IL-4 regulates Th2 cell proliferation.

作者信息

Zhu Jinfang, Guo Liying, Min Booki, Watson Cynthia J, Hu-Li Jane, Young Howard A, Tsichlis Philip N, Paul William E

机构信息

Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Immunity. 2002 May;16(5):733-44. doi: 10.1016/s1074-7613(02)00317-5.

DOI:10.1016/s1074-7613(02)00317-5

PMID:12049724

Abstract

IL-4 is important in Th2 differentiation and in cell expansion. Stat6 is necessary and sufficient for both functions. Although Gata3 is critical for Th2 polarization, it is not sufficient to mediate IL-4-driven cell expansion. We report that growth factor independent-1 (Gfi-1), a Stat6-dependent transcriptional repressor, strikingly increases Th2 cell expansion by promoting proliferation and preventing apoptosis. Cells infected with a Gfi-1 retrovirus show striking enhancement of IL-2-induced Stat5 phosphorylation and repression of p27(Kip-1) expression, suggesting a potential mechanism for the Gfi-1 growth effect. The synergy of Gfi-1 and Gata3 provides a mechanism through which IL-4 could selectively promote Th2 cell expansion.

摘要

白细胞介素-4在辅助性T细胞2（Th2）分化和细胞扩增中起重要作用。信号转导子和转录激活子6（Stat6）对于这两种功能都是必需且充分的。尽管Gata3对Th2极化至关重要，但它不足以介导白细胞介素-4驱动的细胞扩增。我们报道，生长因子独立-1（Gfi-1），一种依赖Stat6的转录抑制因子，通过促进增殖和防止细胞凋亡显著增加Th2细胞扩增。感染Gfi-1逆转录病毒的细胞显示白细胞介素-2诱导的Stat蛋白5磷酸化显著增强以及p27（Kip-1）表达受到抑制，提示Gfi-1生长效应的一种潜在机制。Gfi-1和Gata3的协同作用提供了一种机制，通过该机制白细胞介素-4可选择性促进Th2细胞扩增。