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猴疱疹病毒顶端对Lck介导的信号转导的下调作用

Downregulation of Lck-mediated signal transduction by tip of herpesvirus saimiri.

作者信息

Jung J U, Lang S M, Jun T, Roberts T M, Veillette A, Desrosiers R C

机构信息

New England Regional Primate Research Center, Department of Microbiology and Molecular Genetics, Harvard Medical School, Southborough, Massachusetts 01772-9102, USA.

出版信息

J Virol. 1995 Dec;69(12):7814-22. doi: 10.1128/JVI.69.12.7814-7822.1995.

DOI:10.1128/JVI.69.12.7814-7822.1995
PMID:7494293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC189725/
Abstract

A protein, called tip, of herpesvirus saimiri associates with Lck in transformed T cells. To investigate the effects of complex formation on cellular signal transduction, we constructed human Jurkat-T-cell lines expressing tip. The expression of tip in Jurkat-T cells dramatically suppressed cellular tyrosine phosphorylation and surface expression of lymphocyte antigens. The expression of tip also blocked the induction of tyrosine phosphorylation by anti-CD3 stimulation. The expression of tip in fibroblast cells suppressed the transforming activity of oncogenic F505 Lck. Binding assays showed that the SH3 domain of Lck is sufficient to form a stable complex with tip in vitro. These results demonstrate that tip acts at an early stage of the T-cell signal transduction cascade by associating with Lck and downregulating Lck-mediated activation. Inhibition of Lck-mediated signal transduction by tip in T cells appears to be analogous to the inhibition of Lyn/Syk-mediated signal transduction in B cells by LMP2A of the B-cell-tropic Epstein-Barr virus.

摘要

赛氏疱疹病毒的一种名为Tip的蛋白质在转化的T细胞中与Lck相关联。为了研究复合物形成对细胞信号转导的影响，我们构建了表达Tip的人Jurkat - T细胞系。Tip在Jurkat - T细胞中的表达显著抑制了细胞酪氨酸磷酸化以及淋巴细胞抗原的表面表达。Tip的表达还阻断了抗CD3刺激诱导的酪氨酸磷酸化。Tip在成纤维细胞中的表达抑制了致癌性F505 Lck的转化活性。结合试验表明，Lck的SH3结构域在体外足以与Tip形成稳定的复合物。这些结果表明，Tip通过与Lck相关联并下调Lck介导的激活作用于T细胞信号转导级联反应的早期阶段。Tip在T细胞中对Lck介导的信号转导的抑制作用似乎类似于嗜B细胞的爱泼斯坦 - 巴尔病毒的LMP2A对B细胞中Lyn/Syk介导的信号转导的抑制作用。

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