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白细胞涎酸蛋白(CD43)-主要组织相容性复合体I类分子相互作用参与自发T细胞共轭体形成。

Leukosialin (CD43)-major histocompatibility class I molecule interactions involved in spontaneous T cell conjugate formation.

作者信息

Stöckl J, Majdic O, Kohl P, Pickl W F, Menzel J E, Knapp W

机构信息

Institute of Immunology, University of Vienna, Austria.

出版信息

J Exp Med. 1996 Nov 1;184(5):1769-79. doi: 10.1084/jem.184.5.1769.

DOI:10.1084/jem.184.5.1769
PMID:8920865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2192875/
Abstract

Resting T cells spontaneously adhere in a selective manner to potent accessory cells, such as dendritic cells (DC) and lymphoblastoid B blasts (LCL). Here we demonstrate that leukosialin (CD43) and major histocompatibility complex class I molecules (MHC-I) might play a critical role in this process. T cell conjugate formation with monocyte-derived DC (md-DC) and LCL could be strongly inhibited by either preincubating T cells with Fab fragments of CD43 monoclonal antibody (mAb) 6F5 or by preincubating md-DC or LCL with MHC-I mAb W6/32. Intact CD43 mAb 6F5, in contrast to monovalent Fab fragments, enhanced T cell adhesiveness by transactivating CD2 binding to CD58 molecules. Interestingly, induction of this proadhesive signal via CD43 with intact 6F5 mAb was found to revert mAb W6/32-mediated inhibition of T cell conjugate formation. These observations indicated that CD43 cross-linkage mimics and monovalent mAb 6F5 inhibits interaction of T cell CD43 with a stimulatory ligand on opposing cells, presumably MHC-I. For the demonstration of direct physical interaction between CD43 on T cells and MHC-I-coated beads it was necessary, however, to ligate CD2 on T cells with a stimulatory pair of CD2 mAbs (VIT13 plus TS2/18). This suggests that CD2 ligation crosswise upregulates CD43 binding avidity for MHC-I and that both adhesion molecule pairs (CD43/MHC-I and CD2/CD58) act in concert to induce and mediate T cell conjugate formation with certain cell types.

摘要

静息T细胞会以选择性方式自发黏附于强大的辅助细胞,如树突状细胞(DC)和成淋巴细胞样B母细胞(LCL)。在此我们证明,白细胞唾液酸蛋白(CD43)和主要组织相容性复合体I类分子(MHC-I)可能在此过程中发挥关键作用。T细胞与单核细胞衍生的DC(md-DC)和LCL形成结合物的过程可通过以下两种方式被强烈抑制:一是用CD43单克隆抗体(mAb)6F5的Fab片段预孵育T细胞,二是用MHC-I mAb W6/32预孵育md-DC或LCL。与单价Fab片段相反,完整的CD43 mAb 6F5通过反式激活CD2与CD58分子的结合来增强T细胞黏附性。有趣的是,发现用完整的6F5 mAb通过CD43诱导这种促黏附信号可逆转mAb W6/32介导的T细胞结合物形成抑制。这些观察结果表明,CD43交联模拟物和单价mAb 6F5抑制T细胞CD43与相对细胞上的刺激性配体(可能是MHC-I)的相互作用。然而,为了证明T细胞上的CD43与包被有MHC-I的珠子之间的直接物理相互作用,有必要用一对刺激性的CD2 mAb(VIT13加TS2/18)连接T细胞上的CD2。这表明CD2交联向上调节CD43对MHC-I的结合亲和力,并且这两个黏附分子对(CD43/MHC-I和CD2/CD58)协同作用以诱导和介导T细胞与某些细胞类型形成结合物。

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