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首页> 外文期刊>Molecular and Cellular Biology >HIP-55 Is Important for T-Cell Proliferation, Cytokine Production, and Immune Responses
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HIP-55 Is Important for T-Cell Proliferation, Cytokine Production, and Immune Responses

机译：HIP-55对T细胞增殖，细胞因子生成和免疫反应很重要

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Engagement of the T-cell receptor (TCR) triggers a series of signaling events that lead to the activation of T cells. HIP-55 (SH3P7 or mAbp1), an actin-binding adaptor protein, interacts with and is tyrosine phosphorylated by ZAP-70, which is a crucial proximal protein tyrosine kinase for TCR signaling. HIP-55 is important for JNK and HPK1 activation induced by TCR signaling. In this study, we report the generation and characterization of HIP-55 knockout mice. We found that HIP-55 knockout mice were viable and fertile but showed decreased body weight and increased occurrence of death within the first 4 weeks after birth. The lymphoid organs in HIP-55 knockout mice showed cellularity and T-cell development comparable to that of the wild-type mice. HIP-55 knockout T cells displayed defective T-cell proliferation, decreased cytokine production, and decreased up-regulation of the activation markers induced by TCR stimulation. TCR internalization was slightly increased in HIP-55 knockout T cells. These phenotypes were accompanied by reduced immune responses, including antigen-specific antibody production and T-cell proliferation in HIP-55 knockout mice. The TCR-induced signaling events, including LAT/phospholipase Cγ1 phosphorylation and HPK1/JNK activation, were partially defective in HIP-55 knockout T cells. These results demonstrate the importance of HIP-55 as an adaptor protein in the TCR signaling and immune system.
机译：T细胞受体（TCR）的参与触发了一系列信号事件，导致T细胞活化。 HIP-55（SH3P7或mAbp1）是一种肌动蛋白结合衔接蛋白，可与ZAP-70相互作用并被酪氨酸磷酸化，ZAP-70是TCR信号转导的关键近端蛋白酪氨酸激酶。 HIP-55对于由TCR信号诱导的JNK和HPK1激活很重要。在这项研究中，我们报告了HIP-55基因敲除小鼠的产生和特征。我们发现，HIP-55基因敲除小鼠是活的和可育的，但在出生后的前4周内体重下降，死亡发生率增加。 HIP-55基因敲除小鼠的淋巴器官显示出与野生型小鼠相当的细胞性和T细胞发育。 HIP-55基因敲除的T细胞表现出缺陷的T细胞增殖，减少了细胞因子的产生，并减少了由TCR刺激诱导的激活标记的上调。在HIP-55基因敲除的T细胞中，TCR的内在化略有增加。这些表型伴随着免疫反应的降低，包括HIP-55基因敲除小鼠的抗原特异性抗体产生和T细胞增殖。 TCR诱导的信号转导事件，包括LAT /磷脂酶Cγ1磷酸化和HPK1 / JNK激活，在HIP-55基因敲除的T细胞中部分缺陷。这些结果证明了HIP-55作为TCR信号传导和免疫系统中的衔接蛋白的重要性。

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