L3T4在T细胞活化中的作用:L3T4可能既是一种ia结合蛋白,也是一种转导负信号的受体。

J P Tite, A Sloan, C A Janeway
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引用次数: 0

摘要

T细胞表面分子Lyt-2和L3T4与携带它们的T细胞识别的MHC基因产物的类别密切相关。L3T4分子被认为在增强特异性T细胞对抗原Ia的识别中起作用。在本实验中,我们通过检测L3T4特异性单克隆抗体GK1.5在存在或不存在ii类mhc基因产物时对T细胞反应的影响,探索了L3T4在T细胞活化中的作用。我们的研究表明,GK1.5在缺乏ii类mhc基因产物的情况下抑制T细胞活化,而针对其他T细胞表面分子的抗体不会向相同的细胞转导负信号。我们将我们的结果解释为提示L3T4的信号作用,并由此推断Lyt-2也是如此。我们认为ii类限制性T细胞上的L3T4分子启动了L3T4+ T细胞与其携带ii类mhc基因产物的靶细胞(B细胞,APC)之间的相互作用。这种初始接触对于允许抗原、Ia和T细胞受体在有限时间内形成激活复合物非常重要,激活复合物反过来将显性信号转导到细胞。在缺乏特异性抗原的情况下,或者如果II类携带细胞具有错误的MHC基因型,使得抗原:Ia受体不能聚集,那么L3T4与II类分子的结合将向T细胞传递一个净负信号。我们认为,在这种情况下,这种负信号负责T细胞:靶细胞解偶联。因此,我们建议L3T4启动携带Ia的T细胞相互作用,并在有限时间后向T细胞发出信号停止相互作用,除非存在刺激水平的抗原:Ia复合物,而T细胞的受体是特异性的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of L3T4 in T cell activation: L3T4 may be both an Ia-binding protein and a receptor that transduces a negative signal.

The T cell surface molecules Lyt-2 and L3T4 are strongly correlated with the class of MHC gene product recognized by the T cell bearing them. The L3T4 molecule has been proposed to play a role in enhancing recognition of antigen:Ia by specific T cells. In the present experiments, we have explored the role of L3T4 in T cell activation by examining the effects of the L3T4-specific monoclonal antibody GK1.5 on T cell responses in the presence or absence of class II-MHC gene products. Our studies show that GK1.5 inhibits T cell activation in the absence of class II-MHC gene products, while antibodies to other T cell surface molecules do not transduce negative signals to the same cells. We interpret our results as suggesting a signaling role for L3T4 and, by inference, for Lyt-2 as well. We would propose that L3T4 molecules on the class II-restricted T cell initiate the interaction between the L3T4+ T cell and its class II-MHC gene product bearing target cell (B cell, APC). This initial contact is important in allowing a finite time for antigen, Ia, and the T cell receptor to form an activating complex, which in turn transduces a dominant on signal to the cell. In the absence of specific antigen, or if the class II-bearing cell is of the wrong MHC genotype, so that the antigen:Ia receptor is not aggregated, then the association of L3T4 with class II molecules transduces a net negative signal to the T cell. We suggest that this negative signal is responsible for T cell:target cell deconjugation under these circumstances. Thus, we would propose that L3T4 initiates T cell:Ia-bearing cell interactions and, a finite time later, signals the T cell to discontinue the interaction unless a stimulating level of the antigen:Ia complexes for which the T cell's receptor is specific is present.

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