{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chiurchiu V"],"funding":["Ministero della Salute","Ministero dell'Istruzione, dell'Universita; e della Ricerca","NIH","FISM","European Federation of Immunological Societies_Immunology Letters (EFIS-IL)","NIGMS NIH HHS","Fondazione Italiana Sclerosi Multipla (FISM)"],"pagination":["353ra111"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5149396"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(353)"],"pubmed_abstract":["Resolution of inflammation is a finely regulated process mediated by specialized proresolving lipid mediators (SPMs), including docosahexaenoic acid (DHA)-derived resolvins and maresins. The immunomodulatory role of SPMs in adaptive immune cells is of interest. We report that D-series resolvins (resolvin D1 and resolvin D2) and maresin 1 modulate adaptive immune responses in human peripheral blood lymphocytes. These lipid mediators reduce cytokine production by activated CD8(+) T cells and CD4(+) T helper 1 (TH1) and TH17 cells but do not modulate T cell inhibitory receptors or abrogate their capacity to proliferate. Moreover, these SPMs prevented naïve CD4(+) T cell differentiation into TH1 and TH17 by down-regulating their signature transcription factors, T-bet and Rorc, in a mechanism mediated by the GPR32 and ALX/FPR2 receptors; they concomitantly enhanced de novo generation and function of Foxp3(+) regulatory T (Treg) cells via the GPR32 receptor. These results were also supported in vivo in a mouse deficient for DHA synthesis (Elovl2(-/-)) that showed an increase in TH1/TH17 cells and a decrease in Treg cells compared to wild-type mice. Additionally, either DHA supplementation in Elovl2(-/-) mice or in vivo administration of resolvin D1 significantly reduced cytokine production upon specific stimulation of T cells. These findings demonstrate actions of specific SPMs on adaptive immunity and provide a new avenue for SPM-based approaches to modulate chronic inflammation."],"journal":["Science translational medicine"],"pubmed_title":["Proresolving lipid mediators resolvin D1, resolvin D2, and maresin 1 are critical in modulating T cell responses."],"pmcid":["PMC5149396"],"funding_grant_id":["RF-2011-02346771","R37 GM038765","GM38765","2013/R/8","P01 GM095467","2015/R/8","R01 GM038765","2013/R/2","P01GM095467","2010-2011"],"pubmed_authors":["Maccarrone M","Chiurchiu V","Dalli J","Battistini L","Leuti A","Serhan CN","Jacobsson A"],"additional_accession":[]},"is_claimable":false,"name":"Proresolving lipid mediators resolvin D1, resolvin D2, and maresin 1 are critical in modulating T cell responses.","description":"Resolution of inflammation is a finely regulated process mediated by specialized proresolving lipid mediators (SPMs), including docosahexaenoic acid (DHA)-derived resolvins and maresins. The immunomodulatory role of SPMs in adaptive immune cells is of interest. We report that D-series resolvins (resolvin D1 and resolvin D2) and maresin 1 modulate adaptive immune responses in human peripheral blood lymphocytes. These lipid mediators reduce cytokine production by activated CD8(+) T cells and CD4(+) T helper 1 (TH1) and TH17 cells but do not modulate T cell inhibitory receptors or abrogate their capacity to proliferate. Moreover, these SPMs prevented naïve CD4(+) T cell differentiation into TH1 and TH17 by down-regulating their signature transcription factors, T-bet and Rorc, in a mechanism mediated by the GPR32 and ALX/FPR2 receptors; they concomitantly enhanced de novo generation and function of Foxp3(+) regulatory T (Treg) cells via the GPR32 receptor. These results were also supported in vivo in a mouse deficient for DHA synthesis (Elovl2(-/-)) that showed an increase in TH1/TH17 cells and a decrease in Treg cells compared to wild-type mice. Additionally, either DHA supplementation in Elovl2(-/-) mice or in vivo administration of resolvin D1 significantly reduced cytokine production upon specific stimulation of T cells. These findings demonstrate actions of specific SPMs on adaptive immunity and provide a new avenue for SPM-based approaches to modulate chronic inflammation.","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Aug","modification":"2025-04-26T14:43:11.065Z","creation":"2019-03-27T02:31:13Z"},"accession":"S-EPMC5149396","cross_references":{"pubmed":["27559094"],"doi":["10.1126/scitranslmed.aaf7483"]}}