Regulatory T cell induction during XXXX infection modifies the clinical course of experimental autoimmune encephalomyelitis.

@entity1 @entity3026 @entity21552 @entity66 @entity641 @entity19 @entity1198 @entity1618 @entity281 @entity792 @entity5895 @entity6503 @entity636 @entity15
BACKGROUND: @entity6503 ( @entity6503 ) is used as an animal model for @entity1 @entity15 ( @entity15 ), which is an inflammatory demyelinating @entity3026 characterized by activation of @entity1198 and/or Th17 cells. @entity1 @entity792 can be either exacerbated or suppressed by infectious agents. Recent studies have shown that regulatory T cells play a crucial role in the escape mechanism of @entity21552 spp. both in @entity1 and in experimental models. These cells suppress the @entity1198 response against the parasite and prevent its elimination. Regulatory T cells have been largely associated with protection or amelioration in several @entity792 , mainly by their capacity to suppress proinflammatory response. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we verified that CD4(+)CD25(+) regulatory T cells (T regs) generated during @entity281 (6 days after @entity6503 induction) interfere with the evolution of @entity6503 . We observed a positive correlation between the reduction of @entity6503 clinical symptoms and an increase of @entity5895 levels. @entity66 was also accompanied by a decrease in the expression of @entity636 and IFN-y and increases in the expression of @entity1618 and @entity641 relative to @entity6503 control @entity19 . The adoptive transfer of CD4(+)CD25(+) cells from @entity21552 -infected @entity19 reduced the clinical evolution of @entity6503 , confirming the role of these T regs. CONCLUSIONS/SIGNIFICANCE: These data corroborate previous findings showing that infections interfere with the prevalence and evolution of @entity792 by inducing regulatory T cells, which regulate @entity6503 in an apparently non-specific manner.
