The mechanism by which T cells signal other T cells is not well defined. This was investigated by studying the ability of circulating T cells to induce the proliferation of autologous T cell clones. Peripheral blood T cells activated by cross-linking of the CD3/T cell receptor complex, which increased the expression of cell adhesion molecules LFA-1, LFA-3 and ICAM-1, induced the proliferation of autologous T cell clones. Irradiated antigen-activated peripheral blood T cells could also induce the proliferation of T cell clones which could not recognize that antigen. T-T cell activation required cell contact, was not major histocompatibility complex (MHC) restricted and was blocked by monoclonal antibodies directed against adhesion molecules CD2 and LFA-3 but was not blocked by antibody to class II MHC determinants. As CD2 is the natural ligand for LFA-3, increased expression of T cell surface adhesion molecules LFA-1, ICAM-1 and particularly LFA-3 during an inflammatory response may rapidly recruit T cells that are activated through the CD2 pathway. These results allow a simplified model to explain how relatively few antigen/MHC-specific T cells can recruit large numbers of non-antigen-specific T cells in the generation of an inflammatory response and postulates a novel role of the CD2 molecule in T cell immune function.

译文

:T细胞向其他T细胞发出信号的机制尚不明确。通过研究循环T细胞诱导自体T细胞克隆增殖的能力,对此进行了研究。通过CD3 / T细胞受体复合物交联而活化的外周血T细胞增加了细胞粘附分子LFA-1,LFA-3和ICAM-1的表达,诱导了自体T细胞克隆的增殖。辐射的抗原活化的外周血T细胞也可以诱导不能识别该抗原的T细胞克隆的增殖。 T-T细胞活化需要细胞接触,不受主要组织相容性复合物(MHC)的限制,并且被针对粘附分子CD2和LFA-3的单克隆抗体所阻断,但未被II类MHC决定簇的抗体所阻断。由于CD2是LFA-3的天然配体,因此在炎症反应期间T细胞表面粘附分子LFA-1,ICAM-1尤其是LFA-3的表达增加,可能会迅速募集通过CD2途径激活的T细胞。这些结果使简化的模型可以解释相对较少的抗原/ MHC特异性T细胞在炎症反应的产生中如何募集大量非抗原特异性T细胞,并推测CD2分子在T细胞免疫中的新作用功能。

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