Gaur A, Ruberti G, Haspel R, Mayer J P, Fathman C G
Department of Medicine, Stanford University School of Medicine, CA 94305.
Science. 1993 Jan 1;259(5091):91-4. doi: 10.1126/science.8418501.
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.
在大鼠中进行的T细胞受体（TCR）疫苗接种可预防实验性自身免疫性脑脊髓炎（EAE）的发生，EAE是多发性硬化症的一种动物模型。通过用TCR Vβ8.2基因可变区的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。由于诱导了特异性克隆无反应性（失能），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抑制。在TCR肽疫苗接种前清除CD8 +细胞可阻止这种抑制作用。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。
