Rajagopal K, Sommers C L, Decker D C, Mitchell E O, Korthauer U, Sperling A I, Kozak C A, Love P E, Bluestone J A
Committee on Immunology, University of Chicago, Chicago, Illinois 60637, USA.
J Exp Med. 1999 Dec 6;190(11):1657-68. doi: 10.1084/jem.190.11.1657.
A novel T cell-specific adaptor protein, RIBP, was identified based on its ability to bind Rlk/Txk in a yeast two-hybrid screen of a mouse T cell lymphoma library. RIBP was also found to interact with a related member of the Tec family of tyrosine kinases, Itk. Expression of RIBP is restricted to T and natural killer cells and is upregulated substantially after T cell activation. RIBP-disrupted knockout mice displayed apparently normal T cell development. However, proliferation of RIBP-deficient T cells in response to T cell receptor (TCR)-mediated activation was significantly impaired. Furthermore, these activated T cells were defective in the production of interleukin (IL)-2 and interferon gamma, but not IL-4. These data suggest that RIBP plays an important role in TCR-mediated signal transduction pathways and that its binding to Itk and Rlk/Txk may regulate T cell differentiation.
一种新型的T细胞特异性衔接蛋白RIBP，是在对小鼠T细胞淋巴瘤文库进行酵母双杂交筛选时，基于其与Rlk/Txk结合的能力而被鉴定出来的。还发现RIBP与酪氨酸激酶Tec家族的一个相关成员Itk相互作用。RIBP的表达仅限于T细胞和自然杀伤细胞，并且在T细胞活化后显著上调。RIBP基因敲除小鼠的T细胞发育明显正常。然而，RIBP缺陷型T细胞对T细胞受体（TCR）介导的活化反应的增殖能力显著受损。此外，这些活化的T细胞在白细胞介素（IL）-2和干扰素γ的产生方面存在缺陷，但IL-4的产生没有缺陷。这些数据表明，RIBP在TCR介导的信号转导途径中起重要作用，并且其与Itk和Rlk/Txk的结合可能调节T细胞分化。
