@entity4600 reduces suppressive and migratory functions of XXXX + @entity2902 + regulatory T-cells.

@entity5204 @entity844 @entity404 @entity4600 @entity993 @entity1200 @entity4601 @entity16952 @entity403 @entity2533 @entity2902 @entity4386 @entity688 @entity13525 @entity1366 @entity8110 @entity436
@entity1200 is one of the fundamental aspects of the immune system. The @entity404 (+) @entity2902 (+) regulatory T (Treg) cells have emerged as key players in the development of tolerance to self and foreign antigens. However, little is known about the endogenous factors and mechanisms controlling their suppressive capacity on immune response. In this study, we observed that @entity4600 ( @entity4601 ), an n-3 @entity5204 , diminished, in a dose-dependent manner, the capacity of Treg cells to inhibit the @entity404 (+) @entity2902 (-) effector T-cell proliferation. @entity4601 not only reduced the migration of Treg cells toward chemokines but also downregulated the mRNA expression of @entity16952 and @entity436 in Treg cells. @entity4601 also curtailed @entity1366 and Akt phosphorylation and downregulated the @entity8110 levels in these cells. Contradictorily, @entity4601 upregulated the mRNA expression of @entity403 , @entity4386 , @entity2533 , and @entity688 ; nonetheless, this @entity844 increased the expression of @entity993 ( @entity13525 ) mRNA, known to be involved in Treg cell unresponsiveness. In @entity403 -immunoprepitated nuclear proteins, @entity4601 upregulated histone desacetylase 7 levels that would again participate in the unresposnsiveness of these cells. Finally, a @entity4601 -enriched diet also diminished, ex vivo, the suppressive capacity of Treg cells. Altogether, these results suggest that @entity4601 , by diminishing Treg cell functions, may play a key role in health and disease.
