Weilbach F X, Jung S, Hartung H P, Toyka K V, Giegerich G
Department of Neurology, Julius-Maximilians-Universität, Würzburg, Germany.
J Neuroimmunol. 1997 Oct;79(1):69-75. doi: 10.1016/s0165-5728(97)00112-4.
In experimental autoimmune neuritis (EAN), peripheral nerves are infiltrated by T-lymphocytes and macrophages. By RT-PCR and sequence analysis we characterized TCR V beta-element usage in sciatic nerve tissue of Lewis rats suffering from EAN induced by immunization with peripheral myelin antigens. Several TCR V beta-chain sequences were detected, which did not show homology to sequences of P2-reactive T cells published so far. In EAN induced with peripheral nerve myelin, but not with P2-protein or P2 peptide aa 53-78, TCR V beta 8.2 sequences identical to sequences of encephalitogenic myelin basic protein (MBP) reactive T-cells were identified. These results provide further evidence for a contribution of MBP-directed T-cell reactivity to the pathogenesis of myelin induced EAN and may have implications for the pathogenesis of human demyelinating neuropathies.
在实验性自身免疫性神经炎（EAN）中，外周神经被T淋巴细胞和巨噬细胞浸润。通过逆转录聚合酶链反应（RT-PCR）和序列分析，我们对用外周髓磷脂抗原免疫诱导的EAN的Lewis大鼠坐骨神经组织中TCR Vβ元件的使用情况进行了表征。检测到几个TCR Vβ链序列，它们与迄今公布的P2反应性T细胞序列没有同源性。在用外周神经髓磷脂诱导的EAN中，但在用P2蛋白或P2肽aa 53-78诱导的EAN中未检测到，鉴定出与致脑炎性髓鞘碱性蛋白（MBP）反应性T细胞序列相同的TCR Vβ8.2序列。这些结果为MBP定向的T细胞反应性对髓磷脂诱导的EAN发病机制的贡献提供了进一步的证据，并且可能对人类脱髓鞘性神经病的发病机制有影响。
