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PMID: 9846830 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1.

Journal of neuroimmunology ·Vol. 91 ·No. 1-2 ·1998-11-02 ·Pages 135-46

Aharoni R, Teitelbaum D, Sela M, Arnon R

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.

MeSH Terms
Animals Clone Cells Cross Reactions Cytokines/immunology Encephalomyelitis, Autoimmune, Experimental/chemically induced,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,pharmacology Peptide Fragments/immunology,pharmacology Peptides/immunology Th2 Cells/chemistry,cytology,immunology
Chemicals
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
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Aharoni R
Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel.
Teitelbaum D
Sela M
Arnon R
Article Info
Journal
Journal of neuroimmunology
Abbr.
J Neuroimmunol
ISSN
0165-5728
Published
1998-11-02
Pages
135-46
Language
English
Region
Netherlands
NLM ID
8109498
Subset
IM
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