Smeltz R B, Wolf N A, Swanborg R H
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
J Neuroimmunol. 1998 Jul 1;87(1-2):43-8. doi: 10.1016/s0165-5728(98)00050-2.
We studied synthetic peptides that correspond to two regions of the guinea pig myelin basic protein (MBP) molecule which elicit experimental autoimmune encephalomyelitis (EAE) in DA rats. Using truncated peptides, we determined that two encephalitogenic epitopes reside within MBP63-81, a major determinant defined by MBP residues, 63-76, and a minor encephalitogenic epitope defined by residues, 66-81. Experiments with alanine-substituted analogs of MBP63-76 revealed that the HYGSLP sequence is critical for encephalitogenicity. The core epitope within a second encephalitogenic region, MBP101-120, was defined by residues, 106-119. Studies with analogs of this sequence indicated that residues, Leu 111, Phe 114 and Trp 116 are important for T-cell responsiveness.
我们研究了与豚鼠髓鞘碱性蛋白（MBP）分子的两个区域相对应的合成肽，这两个区域在DA大鼠中引发实验性自身免疫性脑脊髓炎（EAE）。使用截短的肽段，我们确定两个致脑炎表位位于MBP63 - 81内，一个主要的决定簇由MBP残基63 - 76界定，一个次要的致脑炎表位由残基66 - 81界定。对MBP63 - 76丙氨酸取代类似物的实验表明，HYGSLP序列对致脑炎作用至关重要。第二个致脑炎区域MBP101 - 120内的核心表位由残基106 - 由残基106 - 119界定。对该序列类似物的研究表明，残基Leu 111、Phe 114和Trp 116对T细胞反应性很重要。
