Kira J, Bacon M L, Martenson R E, Deibler G E, Kies M W, Alvord E C
J Neuroimmunol. 1986 Sep;12(3):183-93. doi: 10.1016/s0165-5728(86)80002-9.
Experimental allergic encephalomyelitis could be induced in rabbits by injection in Freund's complete adjuvant of either peptide 1-44 or peptide 45-87 of rabbit myelin basic protein. In order to localize the encephalitogenic determinant present in peptide 1-44, several smaller derivative peptides were prepared and examined. Peptic peptide 15-44 and thrombic peptide 1-31 were as active as peptide 1-44, whereas peptic peptides 1-14 and 18-38 and BrCN peptide 22-44 were virtually inactive. Weak activity was shown by BrCN peptide 1-21. These results provide evidence that a major encephalitogenic determinant present in peptide 1-44 lies within sequence 15-31. The encephalitogenic activity of peptide 15-44 was essentially destroyed by oxidation of methionine-21 to methionine sulfoxide; methylation of Met-21, on the other hand, appeared to be relatively ineffective in eliminating the encephalitogenicity of peptide 1-44.
通过在弗氏完全佐剂中注射兔髓鞘碱性蛋白的1 - 44肽段或45 - 87肽段,可在兔中诱发实验性变应性脑脊髓炎。为了定位1 - 44肽段中存在的致脑炎决定簇,制备并检测了几种较小的衍生肽。胃蛋白酶消化的15 - 44肽段和胰蛋白酶消化的1 - 31肽段与1 - 44肽段活性相同,而胃蛋白酶消化的1 - 14肽段、18 - 38肽段和溴化氰裂解的22 - 44肽段实际上无活性。溴化氰裂解的1 - 21肽段显示出较弱的活性。这些结果证明,1 - 44肽段中存在的主要致脑炎决定簇位于15 - 31序列内。将甲硫氨酸 - 21氧化为甲亚砜基本上消除了15 - 44肽段的致脑炎活性;另一方面,甲硫氨酸 - 21甲基化似乎对消除1 - 44肽段的致脑炎活性效果相对较差。