@entity3413 ameliorates experimental autoimmune XXXX by inhibiting @entity1198 /Th17 response and cellular infiltration.

@entity1 @entity32 @entity650 @entity5737 @entity404 @entity66 @entity3413 @entity19 @entity1198 @entity12868 @entity2533 @entity1651 @entity6503 @entity15 @entity6817
AIM: @entity6503 ( @entity6503 ) is a @entity404 (+)-mediated autoimmune pathology of the central nervous system (CNS) that is used as a model for the study of the @entity1 @entity66 , @entity15 . During the development of @entity6503 , auto-reactive @entity1198 and Th17 @entity404 (+) T cells infiltrate the CNS promoting inflammatory cells recruitment, focal @entity32 and tissue destruction. In this sense, @entity6817 , agents used to lower lipid levels, have recently shown to exert interesting immunomodulatory function. In fact, @entity6817 promote a bias towards a Th2 response, which ameliorates the clinical outcome of @entity6503 . Additionally, @entity3413 can inhibit Th17 differentiation. However, many other effects exerted on the immune system by @entity6817 have yet to be clarified, in particular during neuroinflammation. Thus, the aim of this study was to investigate the effects of @entity3413 on the development of experimental autoimmune @entity1651 . METHODS: @entity19 were immunized with MOG35-55 and @entity6503 severity was assessed daily and scored using a clinical scale. Cytokine secretion by mononuclear cells infiltrating the CNS was evaluated by flow cytometry. RESULTS: @entity3413 (5  mg/kg/day) improved clinical outcome, induced an increase in @entity2533 mRNA expression and inhibited @entity650 , IL-12p40, IL-12p70, @entity5737 and @entity12868 secretion (p  <  0.05). This was accompanied by a significant decrease in CNS inflammatory mononuclear cell infiltration, with reduced frequencies of both @entity1198 and Th17 cells. @entity3413 inhibited the proliferation of T lymphocytes co-cultured with primary microglial cells. CONCLUSIONS: @entity3413 treatment promotes @entity6503 clinical amelioration by inhibiting T cell proliferation and CNS infiltration by pathogenic @entity1198 and Th17 cells.
