Glatiramer acetate increases T- and B -regulatory cells and decreases granulocyte-macrophage colony-stimulating factor (GM-CSF) in an animal model of multiple sclerosis.

Abstract

To identify the mechanisms relevant for the therapeutic effect of glatiramer acetate (GA), we studied T- and B- regulatory cells as well as GM-CSF expression in mice recovered from experimental autoimmune encephalomyelitis (EAE). Selective depletion of Tregs reduced but did not eliminate the ability of GA to ameliorate EAE, indicating a role for additional immune-subsets. The prevalence of Bregs in the periphery and the CNS of EAE-mice increased following GA-treatment. Furthermore, GA downregulated the pathological expression of GM-CSF, on both the protein and mRNA levels. These findings corroborate the broad immunomodulatory mechanism of action of GA in EAE/MS.

• Authors: Rina Aharoni, Raya Eilam, Nofar Schottlender, Lihi Radomir, Sandra Leistner-Segal, Tali Feferman, Dana Hirsch, Michael Sela, Ruth Arnon
• Journal: Journal of neuroimmunology (J Neuroimmunol) Vol. 345 Pg. 577281 (08 15 2020) ISSN: 1872-8421 [Electronic] Netherlands
• PMID: 32534388 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2020 Elsevier B.V. All rights reserved.

Chemical References

• Immunosuppressive Agents
• Glatiramer Acetate
• Granulocyte-Macrophage Colony-Stimulating Factor

Topics

• Animals
• B-Lymphocytes, Regulatory (drug effects, metabolism)
• Disease Models, Animal
• Female
• Glatiramer Acetate (pharmacology, therapeutic use)
• Granulocyte-Macrophage Colony-Stimulating Factor (antagonists & inhibitors, metabolism)
• Immunosuppressive Agents (pharmacology, therapeutic use)
• Mice
• Mice, Inbred C57BL
• Mice, Transgenic
• Multiple Sclerosis (drug therapy, metabolism)
• T-Lymphocytes, Regulatory (drug effects, metabolism)