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Glycans as Key Checkpoints of T Cell Activity and Function

2018-11-27Journal article Open access
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dc.contributor.authorPereira, M.
dc.contributor.authorAlves, I.
dc.contributor.authorVicente, M.
dc.contributor.authorCampar, A.
dc.contributor.authorSilva, M.
dc.contributor.authorPadrão, N.
dc.contributor.authorPinto, V.
dc.contributor.authorFernandes, Â.
dc.contributor.authorDias, A.
dc.contributor.authorPinho, S.
dc.date.accessioned2019-08-26T13:47:29Z
dc.date.available2019-08-26T13:47:29Z
dc.date.issued2018-11-27
dc.description.abstractThe immune system is highly controlled and fine-tuned by glycosylation, through the addition of a diversity of carbohydrates structures (glycans) to virtually all immune cell receptors. Despite a relative backlog in understanding the importance of glycans in the immune system, due to its inherent complexity, remarkable findings have been highlighting the essential contributions of glycosylation in the regulation of both innate and adaptive immune responses with important implications in the pathogenesis of major diseases such as autoimmunity and cancer. Glycans are implicated in fundamental cellular and molecular processes that regulate both stimulatory and inhibitory immune pathways. Besides being actively involved in pathogen recognition through interaction with glycan-binding proteins (such as C-type lectins), glycans have been also shown to regulate key pathophysiological steps within T cell biology such as T cell development and thymocyte selection; T cell activity and signaling as well as T cell differentiation and proliferation. These effects of glycans in T cells functions highlight their importance as determinants of either self-tolerance or T cell hyper-responsiveness which ultimately might be implicated in the creation of tolerogenic pathways in cancer or loss of immunological tolerance in autoimmunity. This review discusses how specific glycans (with a focus on N-linked glycans) act as regulators of T cell biology and their implications in disease.pt_PT
dc.description.sponsorshipThe Institute of Molecular Pathology and Immunology of the University of Porto integrates the i3S research unit, which is partially supported by the Portuguese Foundation for Science and Technology (FCT). This article is a result of the project NORTE-01-0145-FEDER-000029, supported by the Norte Portugal Regional Programme (NORTE 2020) under the PORTUGAL 2020 Partnership Agreement through the European Regional Development Fund. This work was also funded by Fundo Europeu de Desenvolvimento Regional (FEDER) funds through the COMPETE 2020—Operacional Programme for Competitiveness and Internationalization (POCI), Portugal 2020, and by Portuguese funds through the FCT in the framework of the project (POCI-01/ 0145-FEDER-016601 and PTDC/DTP-PIC/0560/2014, as well as POCI-01-0145-FEDER-028772). SSP acknowledges the European Crohn's and Colitis Organization (ECCO) for ECCO Grant 2017, the Broad Medical Research Program at the Crohn's and Colitis Foundation of America, and the Portuguese Group of Study in IBD (GEDII) for funding. MSP [SFRH/BD/110148/2015], IA [SFRH/BD/128874/2017], MV [PD/BD/135452/2017], received funding from the FCpt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationFront Immunol. 2018 Nov 27;9:2754pt_PT
dc.identifier.doi10.3389/fimmu.2018.02754pt_PT
dc.identifier.issn1664-3224
dc.identifier.urihttp://hdl.handle.net/10400.16/2285
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherFrontiers Mediapt_PT
dc.relation.publisherversionhttps://www.frontiersin.org/articles/10.3389/fimmu.2018.02754/fullpt_PT
dc.subjectN-glycosylationpt_PT
dc.subjectglycanspt_PT
dc.subjectT cellspt_PT
dc.subjectimmune responsept_PT
dc.subjectautoimmunitypt_PT
dc.subjectself-tolerancept_PT
dc.titleGlycans as Key Checkpoints of T Cell Activity and Functionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceSwitzerlandpt_PT
oaire.citation.startPage2754pt_PT
oaire.citation.titleFrontiers in Immunologypt_PT
oaire.citation.volume9pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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