Michel F, Acuto O
Molecular Immunology Unit, Department of Immunology, Pasteur Institute, Paris, France.
Cell Immunol. 1996 Nov 1;173(2):165-75. doi: 10.1006/cimm.1996.0264.
T cell adhesion induced after physiological stimulation by antigen was investigated using murine T cell hybridomas specific for a tetanus toxin peptide. By employing a novel assay, the T cell hybridomas were shown to strongly adhere to peptide-pulsed APC in a dose-dependent fashion. Adhesion peaked at 30-60 min and declined thereafter. This assay allowed us to study the relationship between T cell adhesion and later activation responses using tetanus toxin peptide and alanine monosubstituted analogs. We show that the degree of peptide-induced T cell adhesion correlated with the magnitude of late functional responses. CD4, LFA-1 (CD11a/CD18), and CD28 were critical in the adhesion response. The enhancing role of CD4 was further demonstrated by reduced levels of T cell adhesion and late responses of CD4- T cell hybridomas. Reexpression of CD4 reversed these defects. Our data suggest a link between antigen-induced T cell adhesion and late responses and also suggest that signals mediated by TCR and CD4 coengagement may induce a greater activation and/or recruitment of molecules involved in T cell adhesion.
利用针对破伤风毒素肽的小鼠T细胞杂交瘤,研究了抗原在生理刺激后诱导的T细胞黏附。通过采用一种新型检测方法,发现T细胞杂交瘤以剂量依赖方式强烈黏附于肽脉冲处理的抗原呈递细胞(APC)。黏附在30 - 60分钟时达到峰值,随后下降。该检测方法使我们能够利用破伤风毒素肽和丙氨酸单取代类似物研究T细胞黏附与后期激活反应之间的关系。我们发现肽诱导的T细胞黏附程度与后期功能反应的强度相关。CD4、淋巴细胞功能相关抗原-1(LFA-1,CD11a/CD18)和CD28在黏附反应中起关键作用。CD4 - T细胞杂交瘤的T细胞黏附水平降低和后期反应进一步证明了CD4的增强作用。CD4的重新表达逆转了这些缺陷。我们的数据表明抗原诱导的T细胞黏附与后期反应之间存在联系,也表明TCR和CD4共同参与介导的信号可能诱导参与T细胞黏附的分子发生更大程度的激活和/或募集。