Spies J M, Pollard J D, Bonner J G, Westland K W, McLeod J G
Department of Medicine, University of Sydney, NSW, Australia.
J Neuroimmunol. 1995 Mar;57(1-2):77-84. doi: 10.1016/0165-5728(94)00164-j.
Studies were conducted in experimental allergic neuritis (EAN) to evaluate the possible interaction of cellular and humoral immune mechanisms in the demyelinating process. EAN was induced in Lewis rats by passive transfer of T cells reactive to P2 myelin protein or by active immunisation with whole myelin. Animals were then given systemic antimyelin antibody or control serum and assessed clinically, electrophysiologically and with semiquantitative histological studies. Animals given intraperitoneal (i.p.) P2-reactive T cells and systemic antimyelin antibody developed much more severe disease than those given i.p. T cells alone (P < 0.001). In actively immunised animals, the addition of systemic antimyelin antibody did not significantly alter disease severity. We believe the more severe disease in animals receiving T cells and antimyelin antibody reflects synergy between cellular and humoral immune mechanisms whereby neural antigen-specific T cells breach the blood-nerve barrier, allowing demyelinating antibody access to the endoneurium. In EAN induced by active immunisation with whole myelin it is likely that both B and T cell activation occurs and that the more severe demyelination characteristic of this disease reflects the involvement of both humoral and cellular immunity.
开展了实验性变应性神经炎（EAN）研究，以评估细胞免疫机制和体液免疫机制在脱髓鞘过程中可能的相互作用。通过被动转移对P2髓鞘蛋白反应性的T细胞或用全髓鞘进行主动免疫，在Lewis大鼠中诱导出EAN。然后给动物注射全身性抗髓鞘抗体或对照血清，并进行临床、电生理和半定量组织学研究。腹腔注射（i.p.）P2反应性T细胞和全身性抗髓鞘抗体的动物比仅注射i.p. T细胞的动物病情严重得多（P < 0.001）。在主动免疫的动物中，添加全身性抗髓鞘抗体并未显著改变疾病严重程度。我们认为，接受T细胞和抗髓鞘抗体的动物病情更严重，反映了细胞免疫机制和体液免疫机制之间的协同作用，即神经抗原特异性T细胞破坏血神经屏障，使脱髓鞘抗体能够进入神经内膜。在用全髓鞘进行主动免疫诱导的EAN中，B细胞和T细胞可能均被激活，且该疾病更严重的脱髓鞘特征可能反映了体液免疫和细胞免疫均参与其中。
