TCR signaling induces selective exclusion of CD43 from the T cell-antigen-presenting cell contact site.
TCR signaling induces selective exclusion of CD43 from the T cell-antigen-presenting cell contact site.
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DOI：
10.4049/jimmunol.161.12.6459
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发表时间：
1998-12
影响因子：
4.4
通讯作者：
Anne I. Sperling;J. Šedý;N. Manjunath;Abraham Kupfer;B. Ardman;Janis K. Burkhardt
中科院分区：
文献类型：
--
作者：
Anne I. Sperling;J. Šedý;N. Manjunath;Abraham Kupfer;B. Ardman;Janis K. Burkhardt
CD 43是一种高度糖基化的大分子，可以说是T细胞表面上最丰富的分子。然而，CD 43的功能仍不清楚。利用荧光显微镜，我们发现CD 43被排除在T细胞-APC接触位点之外。这种排斥是Ag依赖性的，因为最佳的CD 43排斥需要Ag脉冲的APC，并且因为在没有任何其他受体配体相互作用的情况下，通过CD 3的信号传导可以诱导CD 43的调节。这些数据表明，CD 43可能作为非特异性T细胞-APC相互作用的屏障，其由于T细胞活化而被去除。从相互作用位点排除是CD 43的独特特征，并且并非普遍存在于所有大的高度糖基化分子，因为CD 45未被排除。因此，CD 43可能代表T细胞表面上的一种新的调节分子，其可以通过改变其在细胞表面上的位置来指导T细胞相互作用。
CD43, a large highly glycosylated molecule, is arguably the most abundant molecule on the surface of T cells. Nevertheless, the function of CD43 remains unclear. Utilizing fluorescence microscopy, we find that CD43 is excluded from the T cell-APC contact site. This exclusion is Ag dependent since optimal CD43 exclusion requires Ag-pulsed APC, and since signaling through CD3, in the absence of any other receptor ligand interactions, can induce the modulation of CD43. These data suggest that CD43 may function as a barrier to nonspecific T cell-APC interactions that is removed as a result of T cell activation. Exclusion from the interaction site is a unique feature of CD43 and not universally found for all large highly glycosylated molecules since CD45 is not excluded. Thus, CD43 may represent a novel regulatory molecule on the T cell surface that can direct T cell interactions by changing its location on the cell surface.