抗原诱导的实验性变应性脑脊髓炎的抑制作用。IV. 髓鞘碱性蛋白分子C末端的研究（1）

Antigen-induced inhibition of experimental allergic encephalomyelitis. IV. Studies of the C-terminal end of the myelin basic protein molecule (1).

作者信息

Swanborg R H

出版信息

Immunol Commun. 1975;4(4):387-97. doi: 10.3109/08820137509055788.

DOI:10.3109/08820137509055788

Abstract

The C-terminal end of the myelin basic protein (BP) molecule (peptide 117.170) was obtained by cleavage with BNPS-skatole, and purified by gel filtration. Peptide 117-170 from guinea pig BP induced experimental allergic encephalomyelitis (EAE) in Lewis rats, whereas the corresponding peptide from bovine BP was inactive. Neither peptide showed more than trace activity when tested in guinea pigs. Guinea pigs and rats treated with peptide 117-170 in incomplete Freund adjuvant were not rendered unresponsive to EAE induced by subsequent challenge with an encephalitogenic emulsion of BP in complete Freund adjuvant. Indeed, peptide-pretreated rats tended to develop clinical EAE significantly earlier than untreated controls.

摘要

髓鞘碱性蛋白（BP）分子的C末端（肽段117 - 170）通过用BNPS - 粪臭素裂解获得，并通过凝胶过滤纯化。豚鼠BP的肽段117 - 170在Lewis大鼠中诱发了实验性变应性脑脊髓炎（EAE），而牛BP的相应肽段则无活性。在豚鼠中测试时，两种肽段均未表现出超过微量的活性。用不完全弗氏佐剂中的肽段117 - 170处理的豚鼠和大鼠，对随后用完全弗氏佐剂中的致脑炎BP乳剂攻击诱导的EAE并未产生无反应性。实际上，经肽段预处理的大鼠往往比未处理的对照组显著更早出现临床EAE。