Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8463837 | Cellular Immunology | 2014 | 6 Pages |
Abstract
CD4+ T cells are critical for adaptive immunity. MAP4K4 is a key member of germinal center kinase group. However, the physiological function of MAP4K4 in primary CD4+ T cells is still unclear. In this study, it was demonstrated that in vitro, MAP4K4 deletion remarkably suppressed CD4+ T cell proliferation in response to phorbol 12-myristate 13-acetate (PMA) and ionomycin, which was not due to enhancing cell apoptosis. Additionally, MAP4K4 was required for the activation of CD4+ T cells. MAP4K4 deletion significantly down-regulated expression of interleukin 2 (IL-2) and interferon-γ (IFN-γ), while notably up-regulating the expression of regulatory T cells (Treg) transcription factor Foxp3 in peripheral CD4+ T cells. Furthermore, western blot analysis indicated that CD4+ T cells lacking MAP4K4 failed to phosphorylate Jnk, Erk, p38 and PKC-θ. Thus, our results provide the evidence that MAP4K4 is essential for CD4+ T cell proliferation, activation and cytokine production.
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Authors
Hongpeng Huang, Qiuqiong Tang, Hongqian Chu, Jianjun Jiang, Haizhou Zhang, Weidong Hao, Xuetao Wei,