Wilson D B, Steinman L, Gold D P
San Diego Regional Cancer Center, CA 92121.
Immunol Today. 1993 Aug;14(8):376-80; discussion 380-2. doi: 10.1016/0167-5699(93)90136-9.
Repertoire analyses of activated T-cell populations specific for myelin basic protein, peptides of which cause experimental allergic encephalomyelitis in rats and mice, indicate a very limited utilization of homologous V alpha and V beta genes in both species. However, the encephalitogenic peptide fragments of myelin basic protein represent different domains of the antigen molecule and the MHC restricting elements are different. This finding has lead to an interpretation, the 'V-region disease hypothesis', which suggests that some TCR molecules may have special effector functions in addition to peptide-MHC recognition. On the basis of recent findings with the rat experimental allergic encephalomyelitis model and preliminary studies in human multiple sclerosis, we present a more conservative and conventional interpretation of the association of certain TCR V-region elements with encephalitogenicity.
对髓鞘碱性蛋白特异的活化T细胞群体进行的谱系分析表明，在大鼠和小鼠中，同源Vα和Vβ基因的利用都非常有限，髓鞘碱性蛋白的肽段可在大鼠和小鼠中引发实验性变应性脑脊髓炎。然而，髓鞘碱性蛋白的致脑脊髓炎肽段代表了抗原分子的不同结构域，且MHC限制元件也不同。这一发现导致了一种解释，即“V区疾病假说”，该假说认为，某些TCR分子除了识别肽-MHC外，可能还具有特殊的效应功能。基于大鼠实验性变应性脑脊髓炎模型的最新发现以及对人类多发性硬化症的初步研究，我们对某些TCR V区元件与致脑脊髓炎能力之间的关联提出了一种更为保守和传统的解释。
