Amelioration of relapsing experimental autoimmune encephalomyelitis with altered myelin basic protein peptides involves different cellular mechanisms

被引：105

作者：

Gaur, A ^{[1
]}

Boehme, SA ^{[1
]}

Chalmers, D ^{[1
]}

Crowe, PD ^{[1
]}

Pahuja, A ^{[1
]}

Ling, N ^{[1
]}

Brocke, S ^{[1
]}

Steinman, L ^{[1
]}

Conlon, PJ ^{[1
]}

机构：

[1] STANFORD UNIV,DEPT NEUROL SCI,STANFORD,CA 94305

来源：

JOURNAL OF NEUROIMMUNOLOGY | 1997年 / 74卷 / 1-2期

关键词：

experimental autoimmune encephalomyelitis; myelin basic protein; multiple sclerosis; Th1/Th2; autoimmunity; cytokines; immunotherapy; altered peptide ligands; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; RECEPTOR ANTAGONIST PEPTIDES; MULTIPLE-SCLEROSIS PATIENTS; T-CELLS; PROTEOLIPID PROTEIN; ENCEPHALITOGENIC EPITOPE; CYTOKINE PATTERNS; IMMUNE DEVIATION; LYMPHOCYTE-T; SJL/J MICE;

D O I：

10.1016/S0165-5728(96)00220-2

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

T-cells specific for a region of human myelin basic protein, amino acids 87-99 (hMBP87-99), have been implicated in the development of multiple sclerosis (MS) a demyelinating disease of the central nervous system. Administration of soluble altered peptide ligand (APL), made by substituting native residues with alanine at either positions 91(91K > A or A91) or 97 (97R > A or A97) in the hMBP87-99 peptide, blocked the development of chronic relapsing experimental autoimmune encephalomyelitis (R-EAE), in the SJL mouse. The non-encephalitogenic APL A91, appears to induce cytokine shifts from Th1 to Th2 in the target T-cells, whereas the encephalitogenic superagonist APL A97 causes deletion of the MBP87-99 responsive cells. Thus, single amino acid changes at different positions in the same peptide epitope can lead to APL capable of controlling auto-immune disease by different mechanisms.

引用

页码：149 / 158

页数：10

共 40 条

[1] Die and let live: Eliminating dangerous lymphocytes [J].