Stepaniak J A, Wolf N A, Sun D, Swanborg R H
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
J Neuroimmunol. 1997 Sep;78(1-2):79-85. doi: 10.1016/s0165-5728(97)00084-2.
We investigated T cell epitopes of guinea pig myelin basic protein (MBP) that induce experimental autoimmune encephalomyelitis (EAE) in DA rats, using synthetic peptides that correspond to regions of the guinea pig MBP molecule that are homologous to rat MBP. Four peptides were encephalitogenic when tested in DA rats. MBP63-81, which partially overlaps the dominant encephalitogenic MBP epitope for Lewis (LEW) rats, caused severe EAE in the DA strain but did not elicit EAE in LEW rats. MBP66-81 and MBP63-76 were also encephalitogenic for DA but not LEW rats. MBP79-99 also induced EAE in DA rats, although MBP87-99, the minor encephalitogenic LEW epitope, was inactive. This indicates that part of the 79-86 sequence is necessary for encephalitogenic activity in the DA strain. MBP101-120, and MBP142-167 were also encephalitogenic for DA rats. T cells from DA rats immunized with intact MBP proliferated in response to the whole protein and to MBP79-99, but were not stimulated to a significant extent by the other encephalitogenic peptides, suggesting that these may represent cryptic or subdominant epitopes. However, MBP63-81-specific T cell lines could be isolated by repeated restimulation with peptide, indicating that the peptide-specific T cells were present in DA rats at low frequency.
我们使用与豚鼠髓鞘碱性蛋白（MBP）分子中与大鼠MBP同源区域相对应的合成肽，研究了豚鼠MBP的T细胞表位，这些表位可在DA大鼠中诱发实验性自身免疫性脑脊髓炎（EAE）。在DA大鼠中进行测试时，有四种肽具有致脑炎作用。MBP63 - 81与Lewis（LEW）大鼠的主要致脑炎MBP表位部分重叠，在DA品系中引起严重的EAE，但在LEW大鼠中未引发EAE。MBP66 - 81和MBP63 - 76对DA大鼠也有致脑炎作用，但对LEW大鼠无此作用。MBP79 - 99也能在DA大鼠中诱导EAE，尽管LEW的次要致脑炎表位MBP87 - 99无活性。这表明79 - 86序列的一部分对于DA品系中的致脑炎活性是必需的。MBP101 - 120和MBP142 - 167对DA大鼠也有致脑炎作用。用完整MBP免疫的DA大鼠的T细胞对全蛋白和MBP79 - 99有增殖反应，但对其他致脑炎肽没有明显的刺激反应，这表明这些可能代表隐蔽或次要表位。然而，通过用肽反复再刺激可以分离出MBP63 - 81特异性T细胞系，这表明肽特异性T细胞在DA大鼠中以低频率存在。
