Abstract
It had been demonstrated previously that the administration of transforming growth factor-β1 (TGF-β1) reduced the clinical severity of experimental allergic encephalomyelitis (EAE). Treatment with the related immunosuppressive molecule, TGF-β2, resulted in similar inhibition of T cell activation and proliferation in vitro. Long-term treatment was affective in reducing clinical severity of EAE and the number of relapses in mice receiving either myelin basic protein- or peptide-91-103-specific T cell lines. When examined histologically, mice that had received TGF-β2 demonstrated significantly less inflammation and demyelination in the central nervous system. Examination of other organs demonstrated to pathology or deleterious side effects from long-term TGF-β2 therapy. These findings have relevance for the use of TGF-β2 as a therapeutic agent for the human demyelinating disease, multiple sclerosis.
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