Program in Molecular Pathogenesis, Skirball Institute for Biomolecular Medicine, The Helen L and Martin S Kimmel Center for Biology and Medicine, New York University School of Medicine, New York 10016, USA.
Cold Spring Harb Perspect Biol. 2009 Jul;1(1):a002873. doi: 10.1101/cshperspect.a002873.
The concept of an immunological synapse goes back to the early 1980s with the discovery of the relationship between T-cell antigen receptor mediated Ca(2+) signaling, adhesion, and directed secretion. However, this concept did not gain traction until images were published starting in 1998 that revealed a specific molecular pattern in the interface between T cells and model antigen-presenting cells or supported planar bilayers. The dominant pattern, a ring of adhesion molecules surrounding a central cluster of antigen receptors, was observed in both model systems. Analysis of the origins of this pattern over the past 10 years has presented a solution for a difficult problem in lymphocyte biology--how a highly motile cell can suddenly stop when it encounters a signal delivered by just a few antigenic ligands on the surface of another cell without disabling the sensory machinery of the motile cell. The T lymphocyte actively assembles the immunological synapse pattern following a modular design with roots in actin-myosin-based motility.
免疫突触的概念可以追溯到 20 世纪 80 年代早期,当时发现 T 细胞抗原受体介导的 Ca(2+)信号转导、黏附和定向分泌之间存在关系。然而,直到 1998 年开始发表的图像揭示了 T 细胞与模型抗原呈递细胞或支持的平面双层之间界面的特定分子模式后,这个概念才开始受到关注。在这两个模型系统中都观察到了一个主要模式,即围绕着中央簇抗原受体的环状黏附分子。过去 10 年对这种模式起源的分析为淋巴细胞生物学中的一个难题提供了一个解决方案——当一个高度能动的细胞遇到另一个细胞表面仅由几个抗原配体传递的信号时,它如何能够突然停止,而不会使能动细胞的感觉机制失效。T 淋巴细胞在基于肌动蛋白-肌球蛋白的运动的模块化设计的基础上,主动组装免疫突触模式。