Monomeric class I molecules mediate TCR/CD3ε/CD8 interaction on the surface of T cells
Monomeric class I molecules mediate TCR/CD3ε/CD8 interaction on the surface of T cells
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DOI：
10.4049/jimmunol.167.2.821
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发表时间：
2001-07-15
影响因子：
4.4
通讯作者：
Pease, LR
中科院分区：
文献类型：
--
作者：
Block, MS;Johnson, AJ;Pease, LR
在生理性 T 细胞激活过程中，CD8 和 TCR 均与 MHC I 类分子结合。研究表明，为了实现最佳 T 细胞激活，CD8 必须能够与 TCR 结合的 I 类分子结合。然而，没有直接证据证明 CD8 和 TCR 具有 I 类依赖性关联。使用荧光共振能量转移，我们直接证明单个 I 类分子通过充当 CD8 和 TCR 的对接分子而引起 TCR/CD8 相互作用。此外，我们表明，在 TCR/CD8 关联后，CD3 epsilon 与 CD8 非常接近。这些相互作用不依赖于 T 细胞激活的磷酸化事件特征。因此，MHC I 类分子通过与 CD8 和 TCR 结合，介导 T 细胞膜成分的重组，从而促进细胞活化。
Both CD8 and the TCR bind to MHC class I molecules during physiologic T cell activation. It has been shown that for optimal T cell activation to occur, CD8 must be able to bind the same class I molecule that is bound by the TCR. However, no direct evidence for the class I-dependent association of CD8 and the TCR has been demonstrated. Using fluorescence resonance energy transfer, we show directly that a single class I molecule causes TCR/CD8 interaction by serving as a docking molecule for both CD8 and the TCR. Furthermore, we show that CD3 epsilon is brought into close proximity with CD8 upon TCR/CD8 association. These interactions are not dependent on the phosphorylation events characteristic of T cell activation. Thus, MHC class I molecules, by binding to both CD8 and the TCR, mediate the reorganization of T cell membrane components to promote cellular activation.