MECHANISMS OF HUMAN IN VITRO CELLULAR IMMUNE RESPONSES

对外来抗原的识别过程的研究仍在继续 人类T细胞，特别是关于T细胞表面的作用 细胞毒性T细胞(CTL)相互作用的分子。对民主党的认可 抗原已经被用作使用一组DPw2特异性CTL的模型系统 克隆人。效应器和靶子之间的可见共轭形成 使用一种新的染料组合进行了流式细胞术分析，我们发现 这避免了细胞表面的共价修饰。在我们的系统中 有很强的抗原非特异性结合形成和特异性 杀戮的程度取决于触发的程度。我们相信 抗原-非特异性结合物是一种有用的模型系统，在其中 理解单态细胞表面分子(例如，LFA-1， LFA-2、LFA-3)参与淋巴细胞间的相互作用。关于T3的研究 分子已经证实了它在触发T细胞方面的独特作用。抗T3抗体 固定在试剂板上的它们显示出独特的增强能力 抑制CML；表达抗T3的杂交瘤通过以下方式触发自身溶解 DPw2特异性CTL。令人惊讶的是，抗LFA-1抑制了触发的抗T3 裂解，表明LFA-1甚至在这个异种 绕过特定于抗原的步骤的相互作用。

Studies are continuing on the process of recognition of foreign antigen by human T cells, particularly with respect to the role of T cell surface molecules in cytotoxic T cell (CTL) interaction. Recognition of the DP antigens has been used as a model system using a panel of DPw2-specific CTL clones. Visible conjugate formation between effector and target has been analyzed by flow cytometry using a new dye combination we have identified which avoids covalent modification of the cell surface. In our system there is strong antigen-nonspecific conjugate formation and the specificity of killing is determined at the level of triggering. We believe the antigen-nonspecific conjugates to be a useful model system in which to understand the role of monomorphic cell surface molecules (e.g., LFA-1, LFA-2, LFA-3) in interactions of lymphoid cells. Studies of the T3 molecule have confirmed its unique role in triggering T cells. Anti-T3 immobilized on assay plates show a unique enhancement of their ability to inhibit CML; and anti-T3 expressing hybridomas trigger their own lysis by DPw2-specific CTL. Surprisingly, anti-LFA-1 inhibits anti-T3 triggered lysis, suggesting that LFA-1 plays a crucial role even in this xenogeneic interaction which bypasses antigen-specific steps.