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dc.creatorLazarević, Milica
dc.creatorBattaglia, Giuseppe
dc.creatorJevtić, Bojan
dc.creatorĐedović, Neda
dc.creatorBruno, Valeria
dc.creatorCavalli, Eugenio
dc.creatorMiljković, Đorđe
dc.creatorNicoletti, Ferdinando
dc.creatorMomčilović, Miljana
dc.creatorFagone, Paolo
dc.date.accessioned2020-07-30T12:28:43Z
dc.date.available2020-07-30T12:28:43Z
dc.date.issued2020
dc.identifier.issn2076-3921
dc.identifier.urihttps://www.mdpi.com/2076-3921/9/7/608
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/32664399
dc.identifier.urihttps://ibiss-r.rcub.bg.ac.rs/handle/123456789/3819
dc.description.abstractThe aim of this study was to examine the in vitro effects of the slow-releasing H2S donor GYY4137 on the immune cells involved in the pathogenesis of the central nervous system (CNS) autoimmune disease, multiple sclerosis (MS). GYY4137 specifically potentiated TGF-β expression and production in dendritic cells and significantly reduced IFN-γ and IL-17 production in the lymph node and spinal cord T cells obtained from mice immunized with CNS antigens. Both the proportion of FoxP3+ regulatory CD4+ T cells in the lymph node cells, and the percentage of IL-17+ CD4+ T cells in the spinal cord cells were reduced upon culturing with GYY4137. Interestingly, the peripheral blood mononuclear cells obtained from the MS patients had a lower expression of the H2S-producing enzyme, 3-mercaptopyruvate-sulfurtransferase (MPST), in comparison to those obtained from healthy donors. A significant inverse correlation between the expression of MPST and several pro-inflammatory factors was also observed. Further studies on the relevance of the observed results for the pathogenesis and therapy of MS are warranted.
dc.publisherMDPI AG
dc.relationinfo:eu-repo/grantAgreement/MESTD/inst-2020/200007/RS//
dc.rightsopenAccess
dc.sourceAntioxidants (Basel, Switzerland)
dc.sourceAntioxidants (Basel, Switzerland)
dc.subjectT cells
dc.subjectCarbon monoxide
dc.subjectDendritic cells
dc.subjectExperimental autoimmune encephalomyelitis
dc.subjectHydrogen sulfide
dc.subjectMultiple sclerosis
dc.subjectNitric oxide
dc.subjectRegulatory T cells
dc.titleUpregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis.
dc.typearticleen
dc.rights.licenseBY
dcterms.abstractМомчиловић, Миљана; Лазаревић, Милица; Јевтић, Бојан; Ђедовић, Неда; Цавалли, Еугенио; Миљковић, Ђорђе; Ницолетти, Фердинандо; Фагоне, Паоло; Баттаглиа, Гиусеппе; Бруно, Валериа;
dc.rights.holder© 2020 by the authors. Licensee MDPI, Basel, Switzerland.
dc.citation.issue7
dc.citation.volume9
dc.identifier.doi10.3390/antiox9070608
dc.identifier.pmid32664399
dc.identifier.scopus2-s2.0-85087811841
dc.identifier.wos000558340200001
dc.citation.apaLazarević, M., Battaglia, G., Jevtić, B., Đedović, N., Bruno, V., Cavalli, E., et al. (2020). Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis. Antioxidants (Basel, Switzerland), 9(7), 608.
dc.citation.vancouverLazarević M, Battaglia G, Jevtić B, Đedović N, Bruno V, Cavalli E, Miljković Đ, Nicoletti F, Momčilović M, Fagone P. Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis. Antioxidants (Basel, Switzerland). 2020;9(7):608.
dc.citation.spage608
dc.type.versionpublishedVersion
dc.identifier.fulltexthttp://ibiss-r.rcub.bg.ac.rs/bitstream/id/6680/antioxidants-09-00608-v2.pdf
dc.citation.rankaM21~


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