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Do Th2 cells mediate the effects of glatiramer acetate in experimental autoimmune encephalomyelitis?


, : Do Th2 cells mediate the effects of glatiramer acetate in experimental autoimmune encephalomyelitis?. International Immunology 18(4): 537-544

Mechanisms underlying the clinical benefits of glatiramer acetate (GA) for patients with multiple sclerosis (MS) remain elusive. A prevailing hypothesis is that GA can induce T(h)2-polarized T cells, which cross-recognize myelin-specific epitopes and can inhibit myelin-reactive autoaggression in T(h)1 T cells, a process referred to as 'bystander suppression.' To test whether the efficacy of GA is indeed mediated by T(h)2 T cells, we have utilized an animal model for MS: experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. GA therapy conferred moderate protection from EAE. GA-reactive T cells from these mice were not T(h)2 polarized, and the T(h)1 cytokine reduction of myelin-reactive T cells in GA-treated mice was comparable to that in untreated control mice. Significantly, the protective effects of GA against EAE were also observed in IL-4-, IL-10-deficient and IL-4/IL-10 double-deficient mice. Similar to wild-type mice, GA therapy in IL-4- and IL-10-deficient mice was associated with diminished myelin-reactive T cell expansion and reduced production of myelin antigen-induced IFN-gamma and tumor necrosis factor-alpha. Thus, despite the absence of two prominent T(h)2 cytokines, IL-4 and IL-10, either alone or combined, GA was still beneficial in suppressing EAE. Our results caution against the notion that T(h)2 cells and bystander suppression account for the effect of GA on EAE and suggest that an alternative mechanism may operate in GA-treated MS patients.

US$19.90

PMID: 16481342

DOI: 10.1093/intimm/dxh394


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