Abstract
The synthetic amino acid copolymer, copolymer 1 (Cop 1) induces T suppressor (Ts) lines/clones, which are confined to the Th2 pathway, cross react with myelin basic protein (MBP), but not with other myelin antigens on the level of Th2 cytokine secretion. Nevertheless, Cop 1 Ts cells inhibited the IL-2 response of a proteolipid protein (PLP) specific line. Furthermore, Cop 1 Ts cells ameliorated EAE induced by two unrelated encephalitogenic epitopes of PLP: p139-151 and p178-191, that produced different forms of disease. This bystander suppression demonstrated by the Cop 1 Ts cells may explain the therapeutic effect of Cop 1 in EAE and MS.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Clone Cells
-
Cross Reactions
-
Cytokines / immunology
-
Encephalomyelitis, Autoimmune, Experimental / chemically induced
-
Encephalomyelitis, Autoimmune, Experimental / immunology*
-
Epitopes / immunology
-
Female
-
Glatiramer Acetate
-
Immunosuppressive Agents / immunology*
-
Mice
-
Mice, Inbred BALB C
-
Multiple Sclerosis / immunology
-
Myelin Basic Protein / immunology
-
Myelin Proteolipid Protein / immunology
-
Myelin Proteolipid Protein / pharmacology
-
Peptide Fragments / immunology
-
Peptide Fragments / pharmacology
-
Peptides / immunology*
-
Th2 Cells / chemistry
-
Th2 Cells / cytology
-
Th2 Cells / immunology*
Substances
-
Cytokines
-
Epitopes
-
Immunosuppressive Agents
-
Myelin Basic Protein
-
Myelin Proteolipid Protein
-
Peptide Fragments
-
Peptides
-
myelin proteolipid protein (139-151)
-
myelin proteolipid protein (178-191)
-
Glatiramer Acetate