Resolvin E1 Regulates Th17 Function and T Cell Activation

Resolvin E1 (RvE1) is a specialized pro-resolving lipid mediator derived from eicosapentaenoic acid and plays a critical role in resolving inflammation and tissue homeostasis. T 17 cells are a distinct group of T helper (T ) cells with tissue-destructive functions in autoimmune and chronic inflammat...

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Veröffentlicht in:Frontiers in immunology 2021-03, Vol.12, p.637983-637983
Hauptverfasser: Oner, Fatma, Alvarez, Carla, Yaghmoor, Wael, Stephens, Danielle, Hasturk, Hatice, Firatli, Erhan, Kantarci, Alpdogan
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Sprache:eng
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Zusammenfassung:Resolvin E1 (RvE1) is a specialized pro-resolving lipid mediator derived from eicosapentaenoic acid and plays a critical role in resolving inflammation and tissue homeostasis. T 17 cells are a distinct group of T helper (T ) cells with tissue-destructive functions in autoimmune and chronic inflammatory diseases the secretion of IL-17. Dendritic cell (DC)-mediated antigen presentation regulates the T 17-induced progression of inflammation and tissue destruction. In this study, we hypothesized that the RvE1 would restore homeostatic balance and inflammation by targeting the T 17 function. We designed three experiments to investigate the impact of RvE1 on different phases of T 17 response and the potential role of DCs: First CD4 T cells were induced by IL-6/TGF to measure the effect of RvE1 on T 17 differentiation in an inflammatory milieu. Second, we measured the impact of RvE1 on DC-stimulated T 17 differentiation in a co-culture model. Third, we measured the effect of RvE1 on DC maturation. RvE1 blocked the CD25, CCR6 and IL-17 expression; IL-17, IL-21, IL-10, and IL-2 production, suggesting inhibition of T cell activation, T 17 stimulation and chemoattraction. RvE1 also suppressed the activation of DCs by limiting their pro-inflammatory cytokine production. Our findings collectively demonstrated that the RvE1 targeted the T 17 activation and the DC function as a potential mechanism for inflammatory resolution and acquired immune response.
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.637983