KLF4公司
CD8型
生物
细胞毒性T细胞
细胞生物学
T细胞
细胞分化
转录因子
分子生物学
免疫学
免疫系统
体外
生物化学
基因
SOX2
作者
Maksim Mamonkin,Shen Ye,Ping‐Hsien Lee,Monica Puppi,Chun Shik Park,H. Daniel Lacorazza
标识
DOI:10.1016/j.imlet.2013.09.008
摘要
The transcription factor Krüppel-like factor 4 (KLF4) can activate or repress gene expression in a cell-context dependent manner. We have previously shown that KLF4 inhibits the proliferation of naïve CD8+ T cells in vitro downstream of the transcription factor ELF4. In this work, we describe a novel role of KLF4 in the differentiation of CD8+ T cells upon infection. Loss of KLF4 had minimal effect on thymic T cell development and distribution of mature T cells in the spleen, blood, and lymph nodes. KLF4-deficient naïve CD8+ T cells also displayed normal homeostatic proliferation upon adoptive transfer into lymphopenic hosts. However, activation of KLF4-deficient naïve CD8+ T cells by in vitro TCR crosslink and co-stimulation resulted in increased proliferation. Furthermore, naïve KLF4-deficient OT-I CD8+ T cells generated increased numbers of functional memory CD8+ T cells compared to wild type OT-I CD8+ T cells co-injected in the same recipient in both primary and recall responses to Listeria monocytogenes-OVA. Collectively, our data demonstrate that KLF4 regulates differentiation of functional memory CD8+ T cells while sparing development and homeostasis of naïve CD8+ T cells.
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