An altered peptide ligand mediates immune deviation and prevents autoimmune encephalomyelitis
作者： Lindsay B Nicholson , Judith M Greer , Raymond A Sobel , Marjorie B Lees , Vijay K Kuchroo
DOI: 10.1016/1074-7613(95)90169-8
关键词:
摘要: In experimental autoimmune encephalomyelitis (EAE) induced with myelin proteolipid protein (PLP) peptide 139-151, we have previously shown that the disease is mediated by Th1 cells, which recognize tryptophan 144 as primary TCR contact point. Here describe an altered ligand (APL), generated a single amino acid substitution (tryptophan to glutamine) at position (Q144), inhibits development of EAE native PLP 139-151 (W144). We show APL induces T cells are cross-reactive and these produce Th2 (IL-4 IL-10) Th0 (IFN gamma cytokines. Adoptive transfer cell lines confer protection from EAE. These data changing in antigenic can significantly influence differentiation suggest immune deviation may be one mechanisms APLs inhibit disease.
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