Perry L L, Barzaga-Gilbert E, Trotter J L
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840.
J Neuroimmunol. 1991 Jul;33(1):7-15. doi: 10.1016/0165-5728(91)90029-7.
(SJL/J x PL/J)F1 mice immunized with myelin basic protein (MBP) develop an autoimmune demyelinating disease termed relapsing experimental allergic encephalomyelitis (rEAE). The acute state of disease is mediated by CD4+ T cells specific for MBP amino acids 1-9. To determine the immunologic bases for disease relapse, host sensitization to additional autoantigens of the central nervous system was measured. Results indicate that most animals develop T cell reactivity to endogenous myelin proteolipid protein (PLP) during rEAE. However, PLP-specific immunity does not appear to account for expression of relapse episodes of demyelination.
用髓鞘碱性蛋白（MBP）免疫的（SJL/J×PL/J）F1小鼠会患上一种自身免疫性脱髓鞘疾病，称为复发性实验性过敏性脑脊髓炎（rEAE）。疾病的急性期由对MBP氨基酸1 - 9特异的CD4 + T细胞介导。为了确定疾病复发的免疫学基础，检测了宿主对中枢神经系统其他自身抗原的致敏情况。结果表明，大多数动物在rEAE期间会产生针对内源性髓鞘蛋白脂蛋白（PLP）的T细胞反应性。然而，PLP特异性免疫似乎并不能解释脱髓鞘复发发作的表现。
