Higgins P J, Weiner H L
Department of Medicine, Brigham & Women's Hospital, Boston, MA 02115.
J Immunol. 1988 Jan 15;140(2):440-5.
We report that experimental autoimmune encephalomyelitis, a T cell-mediated autoimmune disease studied as a model for multiple sclerosis, can be suppressed in Lewis rats by the oral administration of myelin basic protein (MBP). Both the clinical and histopathologic manifestations of the disease were suppressed in a dose-dependent manner. In addition, proliferative responses to MBP and, to a lesser extent, serum levels of anti-MBP antibody were suppressed by feeding MBP. Suppression of clinical and histologic disease was observed whether animals were fed MBP before or after disease induction, although suppression was more complete when rats were fed before immunization. Disease was also suppressed by the oral administration of either encephalitogenic or nonencephalitogenic fragments and decapeptides of the MBP molecule, with more complete suppression observed when nonencephalitogenic fragments were fed, suggesting that suppressor determinants exist in the MBP molecule distinct from the encephalitogenic region. The oral administration of a non-disease-inducing portion of an autoantigen represents an antigen-specific method by which an experimental autoimmune disease can be immunoregulated.
我们报告称，实验性自身免疫性脑脊髓炎作为多发性硬化症的一种模型进行研究，是一种由T细胞介导的自身免疫性疾病，在Lewis大鼠中通过口服髓鞘碱性蛋白（MBP）可得到抑制。该疾病的临床和组织病理学表现均呈剂量依赖性受到抑制。此外，通过喂食MBP，对MBP的增殖反应以及血清中抗MBP抗体水平在较小程度上也受到抑制。无论动物在疾病诱导之前还是之后喂食MBP，均观察到临床和组织学疾病受到抑制，不过当大鼠在免疫前喂食时抑制更为完全。通过口服MBP分子的致脑炎或非致脑炎片段及十肽也可抑制疾病，当喂食非致脑炎片段时观察到更完全的抑制，这表明在MBP分子中存在与致脑炎区域不同的抑制决定簇。口服自身抗原的非疾病诱导部分代表了一种可对实验性自身免疫性疾病进行免疫调节的抗原特异性方法。
