Logo image
CD8+ T Cells Are Required For Glatiramer Acetate Therapy in Autoimmune Demyelinating Disease
Journal article   Open access   Peer reviewed

CD8+ T Cells Are Required For Glatiramer Acetate Therapy in Autoimmune Demyelinating Disease

Andrew F Tyler, Jason P Mendoza, Mihail Firan and Nitin J Karandikar
PloS one, Vol.8(6), pp.e66772-e66772
06/21/2013
DOI: 10.1371/journal.pone.0066772
PMCID: PMC3689655
PMID: 23805274
url
https://doi.org/10.1371/journal.pone.0066772View
Published (Version of record) Open Access

Abstract

The exact mechanism of glatiramer acetate (GA, Copaxone®), an FDA-approved immunomodulatory therapy for multiple sclerosis (MS), remains unclear after decades of research. Previously, we have shown that GA therapy of MS induces CD8 + T cell responses that can potentially suppress pathogenic CD4 + T cell responses. Using a murine model of MS, experimental autoimmune encephalomyelitis (EAE), we now demonstrate that CD8 + T cells are necessary in mediating the therapeutic effects of GA. Further, adoptive transfer of GA-induced CD8 + T cells resulted in amelioration of EAE, establishing a role as a viable immunotherapy in demyelinating disease. Generation of these cells required indoleamine-2,3-dioxygenase (IDO), while suppressive function depended on non-classical MHC class I, IFN-γ, and perforin expression. GA-induced regulatory myeloid cells, previously shown to activate CD4 + regulatory T cells in an antigen-independent manner, required CD8 + T cells for disease suppression in vivo . These studies demonstrate an essential role for CD8 + T cells in GA therapy and identify their potential as an adoptive immunotherapeutic agent.
Medicine Biology

Details

Metrics

Logo image