TCR-mediated adhesion of T cell hybridomas to planar bilayers containing purified MHC class II/peptide complexes and receptor shedding during detachment.
TCR-mediated adhesion of T cell hybridomas to planar bilayers containing purified MHC class II/peptide complexes and receptor shedding during detachment.
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TCR 介导的 T 细胞杂交瘤与含有纯化的 MHC II 类/肽复合物的平面双层的粘附以及分离过程中受体脱落。
DOI：
10.4049/jimmunol.157.5.2014
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发表时间：
1996
影响因子：
4.4
通讯作者：
E. Unanue
中科院分区：
文献类型：
--
作者：
Michael Loran Dustin;J. Miller;S. Ranganath;D. Vignali;N. Viner;C. Nelson;E. Unanue
T细胞识别外来Ag/MHC II类复合物的灵敏度低至约100个复合物/细胞或约0.2个复合物/微米2。为了更好地理解Ag呈递的识别阶段的物理基础，我们检查了溶菌酶特异性T细胞杂交瘤3A 9与含有共价MHC II类/肽复合物或粘附分子的人工双层的粘附。3A 9细胞的粘附需要MHC II类/肽复合物的超生理密度，并且部分依赖于CD 4;细胞粘附但不爬行。没有观察到粘附到含有MHC II类分子而没有溶菌酶肽的双层。活化的3A 9细胞在含有ICAM-1的双层上粘附和爬行。接触的物理强度用流体剪切测试。粘附于含有MHC II类/肽复合物的双层的3A 9细胞脱落了它们的接触，其保留在基底上并含有TCR。相反，3A 9细胞从ICAM-1双层剥离，并牢固地保持在LFA-1双层上;以依赖于丝状肌动蛋白的方式。当ICAM-1和MHC/肽复合物结合时，3A 9细胞在双层上紧密粘附并扩散，但不爬行，TCR聚集在接触区域的中心。在生理学上，TCR不太可能直接引发粘附。在粘附机制的帮助下形成的TCR簇可能必须脱落以允许去粘附，并且这可能有助于TCR下调。
T cell recognition of foreign Ag/MHC class II complexes is sensitive down to approximately 100 complexes per cell or approximately 0.2 complexes/micron2. To better understand the physical basis of the recognition stage of Ag presentation, we examined adhesion of the lysozyme- specific T cell hybridoma, 3A9, to artificial bilayers containing covalent MHC class II/peptide complexes or adhesion molecules. Adhesion of 3A9 cells required a superphysiologic density of the MHC class II/peptide complex and was partly dependent on CD4; cells adhered but did not crawl. No adhesion was observed to bilayers containing MHC class II molecules without the lysozyme peptide. Activated 3A9 cells adhered and crawled on bilayers containing ICAM-1. The physical strength of contacts was tested with fluid shear. 3A9 cells adherent to bilayers containing MHC class II/peptide complexes shed their contact, which remained on the substrate and contained TCR. In contrast, 3A9 cells peeled from the ICAM-1 bilayer, and held firmly on LFA-1 bilayers; in a manner dependent on filamentous actin. When ICAM-1 and the MHC/peptide complexes were combined, the 3A9 cells adhered tightly and spread, but did not crawl, on the bilayers and TCR clustered at the center of the contact area. Physiologically, the TCR is unlikely to directly initiate adhesion. TCR clusters formed with the assistance of adhesion mechanisms may have to be shed to allow de-adhesion, and this may contribute to TCR down-regulation.