Chu N R, Quaratino S, Feldmann M, Londei M
Kennedy Institute of Rheumatology, Sunley Division, Hammersmith, London, UK.
Int Immunol. 1995 Jul;7(7):1057-63. doi: 10.1093/intimm/7.7.1057.
T cells recognizing tetanus toxin peptide 'p2' (sequence 830-844) raised in HLA DR6 individuals preferentially express V beta 2 in the TCR. A p2-specific T cell line (60% V beta 2+) was used to compare peptide and superantigen [toxic shock syndrome toxin-1 (TSST-1)]-induced clonal anergy. Many experiments consistently revealed that the degree of 'tolerance' or 'clonal anergy' induced by peptide was greater than with the superantigen TSST-1. These results are of interest in a number of contexts. First they suggest that using superantigens or anti-V beta to delete the majority population of T cells may not be sufficient to diminish an autoimmune response. Secondly, the results indicate that induction of anergy of a large proportion of peptide-specific T cells does not lead to a suppressive bystander effect on the remaining responsive T cells. These results emphasize the need to define the dominant autoantigenic epitopes in human autoimmune diseases, since peptide based therapy such as the use of peptide analogues to induce anergy or a change in cytokine profile, is possibly more effective in controlling undesired immune responses than the use of non-antigen, TCR-directed approaches such as superantigens.
在HLA DR6个体中产生的识别破伤风毒素肽“p2”(序列830 - 844)的T细胞在TCR中优先表达Vβ2。使用一个p2特异性T细胞系(60% Vβ2+)来比较肽和超抗原[中毒性休克综合征毒素-1(TSST-1)]诱导的克隆无能。许多实验一致表明,肽诱导的“耐受”或“克隆无能”程度大于超抗原TSST-1。这些结果在许多方面都很有意义。首先,它们表明使用超抗原或抗Vβ来清除大多数T细胞群体可能不足以减弱自身免疫反应。其次,结果表明诱导大部分肽特异性T细胞的无能不会对其余反应性T细胞产生抑制性旁观者效应。这些结果强调了确定人类自身免疫性疾病中主要自身抗原表位的必要性,因为基于肽的疗法,如使用肽类似物诱导无能或改变细胞因子谱,在控制不良免疫反应方面可能比使用非抗原性的、针对TCR的方法(如超抗原)更有效。