Amelioration of relapsing experimental autoimmune encephalomyelitis with altered myelin basic protein peptides involves different cellular mechanisms
作者： Amitabh Gaur , Stefen A Boehme , Derek Chalmers , Paul D Crowe , Anil Pahuja
DOI: 10.1016/S0165-5728(96)00220-2
关键词:
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 multiple sclerosis (MS) demyelinating disease central nervous system. Administration soluble altered peptide ligand (APL), made by substituting native residues with alanine at either positions 91(91K > A or A91) 97 (97R A97) hMBP87-99 peptide, blocked chronic relapsing experimental autoimmune encephalomyelitis (R-EAE), SJL mouse. The non-encephalitogenic APL A91, appears to induce cytokine shifts from Th1 Th2 target T-cells, whereas encephalitogenic superagonist A97 causes deletion MBP87-99 responsive cells. Thus, single acid changes different same epitope can lead capable controlling auto-immune mechanisms.
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