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超抗原诱导的外周T细胞缺失：抗原呈递细胞化学修饰、白细胞介素-4和糖皮质激素的作用。

Superantigen-induced peripheral T-cell deletion: the effects of chemical modification of antigen-presenting cells, interleukin-4 and glucocorticoid hormones.

作者信息

Ayroldi E, Cannarile L, D'Adamio F, Riccardi C

机构信息

Department of Clinical Medicine, Pathology and Pharmacology, Perugia University Medical School, Italy.

出版信息

Immunology. 1995 Apr;84(4):528-35.

PMID:7790025
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1415147/
Abstract

Experiments were performed to evaluate the role of antigen-presenting cells (APC) and the effect of interleukin-4 (IL-4) and glucocorticoid hormone (GCH) exposure on the in vitro deletion of CD4+ CD8- and CD8+ CD4- T cells by staphylococcal enterotoxin B (SEB). APC fixation with the chemical cross-linker 1-ethyl-3-(3-dimethyl-aminopropyl) carbodiimide (ECDI) inhibited their capacity to induce SEB-specific deletion of mature T lymphocytes. Deletion was not influenced by treatment with anti-CD28 antibodies, which modulate T-cell activation. However, it was augmented by IL-4, known to counteract anti-CD3- and GCH-induced thymocyte apoptosis, and was inhibited by dexamethasone (DEX). These results indicate that metabolically active APC are required for deletion of antigen-specific mature T cells and suggest that IL-4 and GCH can modulate this phenomenon in vitro.

摘要

进行实验以评估抗原呈递细胞（APC）的作用以及白细胞介素-4（IL-4）和糖皮质激素（GCH）暴露对葡萄球菌肠毒素B（SEB）体外清除CD4 + CD8-和CD8 + CD4- T细胞的影响。用化学交联剂1-乙基-3-（3-二甲基氨基丙基）碳二亚胺（ECDI）固定APC会抑制其诱导成熟T淋巴细胞SEB特异性清除的能力。用抗CD28抗体处理不影响清除，抗CD28抗体可调节T细胞活化。然而，已知可抵消抗CD3和GCH诱导的胸腺细胞凋亡的IL-4可增强清除作用，而地塞米松（DEX）则抑制清除作用。这些结果表明，代谢活跃的APC是清除抗原特异性成熟T细胞所必需的，并表明IL-4和GCH可在体外调节这一现象。