Krishnan Sandeep, Warke Vishal G, Nambiar Madhusoodana P, Tsokos George C, Farber Donna L
Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
J Immunol. 2003 Apr 15;170(8):4189-95. doi: 10.4049/jimmunol.170.8.4189.
The TCR-mediated signals required to activate resting T cells have been well characterized; however, it is not known how TCR-coupled signals are transduced in differentiated effector T cells that coordinate ongoing immune responses. Here we demonstrate that human effector CD4 T cells up-regulate the expression of the CD3zeta-related FcRgamma signaling subunit that becomes part of an altered TCR/CD3 signaling complex containing CD3epsilon, but not CD3zeta. The TCR/CD3/FcRgamma complex in effector cells recruits and activates the Syk, but not the ZAP-70, tyrosine kinase. This physiologic switch in TCR signaling occurs exclusively in effector, and not naive or memory T cells, suggesting a potential target for manipulation of effector responses in autoimmune, malignant, and infectious diseases.
激活静息T细胞所需的TCR介导信号已得到充分表征；然而，尚不清楚TCR偶联信号在协调正在进行的免疫反应的分化效应T细胞中是如何转导的。在这里，我们证明人类效应CD4 T细胞上调CD3ζ相关的FcRγ信号亚基的表达，该亚基成为包含CD3ε但不包含CD3ζ的改变的TCR/CD3信号复合物的一部分。效应细胞中的TCR/CD3/FcRγ复合物募集并激活Syk酪氨酸激酶，而不是ZAP-70酪氨酸激酶。TCR信号的这种生理转换仅发生在效应T细胞中，而不是幼稚或记忆T细胞中，这表明在自身免疫性、恶性和感染性疾病中操纵效应反应可能有一个潜在靶点。
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