REQUIREMENT FOR CD8+ CELLS IN T-CELL RECEPTOR PEPTIDE-INDUCED CLONAL UNRESPONSIVENESS
REQUIREMENT FOR CD8+ CELLS IN T-CELL RECEPTOR PEPTIDE-INDUCED CLONAL UNRESPONSIVENESS
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DOI：
10.1126/science.8418501
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发表时间：
1993-01-01
期刊：
影响因子：
56.9
通讯作者：
FATHMAN, CG
中科院分区：
文献类型：
--
作者：
GAUR, A;HASPEL, R;FATHMAN, CG
在大鼠中进行T细胞受体（TCR）疫苗接种可阻止实验性自身免疫性脑脊髓炎（EAE，一种多发性硬化症的动物模型）的发展。通过用TCR Vβ8.2基因可变区的一个免疫原性肽片段对小鼠进行疫苗接种，研究了这种潜在免疫疗法的机制。随后，另一种通常诱导由Vβ8.2⁺ T细胞介导的免疫反应的免疫原受到了抑制，因为已诱导出特异性克隆无反应性（失能）。在TCR肽疫苗接种前耗竭CD8⁺细胞可阻断这种抑制作用。因此，克隆失能依赖于CD8⁺ T细胞，并且这种免疫调节性T细胞可能参与EAE的正常病程。
T cell receptor (TCR) vaccination in rats prevents the development of experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis. The mechanism of this potential immunotherapy was examined by vaccinating mice with an immunogenic peptide fragment of the variable region of the TCR V(beta)8.2 gene. Another immunogen that usually induces an immune response mediated by V(beta)8.2+ T cells was subsequently inhibited because specific clonal unresponsiveness (anergy) had been induced. Depletion of CD8+ cells before TCR peptide vaccination blocked such inhibition. Thus, the clonal anergy was dependent on CD8+ T cells, and such immunoregulatory T cells may participate in the normal course of EAE.