Brod S A, Purvee M, Benjamin D, Hafler D A
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
Eur J Immunol. 1990 Oct;20(10):2259-68. doi: 10.1002/eji.1830201015.
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.
T细胞向其他T细胞发出信号的机制尚未明确界定。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探究。通过CD3/T细胞受体复合物交联激活的外周血T细胞，增加了细胞黏附分子LFA-1、LFA-3和ICAM-1的表达，诱导了自体T细胞克隆的增殖。经辐射的抗原激活外周血T细胞也能诱导无法识别该抗原的T细胞克隆的增殖。T-T细胞激活需要细胞接触，不受主要组织相容性复合体（MHC）限制，并且被针对黏附分子CD2和LFA-3的单克隆抗体阻断，但不被针对II类MHC决定簇的抗体阻断。由于CD2是LFA-3的天然配体，在炎症反应期间T细胞表面黏附分子LFA-1、ICAM-1尤其是LFA-3表达的增加可能会迅速募集通过CD2途径激活的T细胞。这些结果提供了一个简化模型，以解释在炎症反应产生过程中相对较少的抗原/MHC特异性T细胞如何能够募集大量非抗原特异性T细胞，并推测了CD2分子在T细胞免疫功能中的新作用。
