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JAK inhibitors and modulation of B cell immune responses in rheumatoid arthritis

2021Artigo científico Acesso aberto
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dc.contributor.authorMoura, Rita
dc.contributor.authorFonseca, João Eurico
dc.date.accessioned2021-03-10T12:17:24Z
dc.date.available2021-03-10T12:17:24Z
dc.date.issued2021
dc.descriptionCopyright © 2021 Moura and Fonseca. This is an open-access article distributed under the terms of the Creative Commons Attribution License(CC BY). The use,distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use,distribution or reproduction is permitted which does not comply with these termspt_PT
dc.description.abstractRheumatoid arthritis (RA) is a chronic, systemic immune-mediated inflammatory disease that can lead to joint destruction, functional disability and substantial comorbidity due to the involvement of multiple organs and systems. B cells have several important roles in RA pathogenesis, namely through autoantibody production, antigen presentation, T cell activation, cytokine release and ectopic lymphoid neogenesis. The success of B cell depletion therapy with rituximab, a monoclonal antibody directed against CD20 expressed by B cells, has further supported B cell intervention in RA development. Despite the efficacy of synthetic and biologic disease modifying anti-rheumatic drugs (DMARDs) in the treatment of RA, few patients reach sustained remission and refractory disease is a concern that needs critical evaluation and close monitoring. Janus kinase (JAK) inhibitors or JAKi are a new class of oral medications recently approved for the treatment of RA. JAK inhibitors suppress the activity of one or more of the JAK family of tyrosine kinases, thus interfering with the JAK-Signal Transducer and Activator of Transcription (STAT) signaling pathway. To date, there are five JAK inhibitors (tofacitinib, baricitinib, upadacitinib, peficitinib and filgotinib) approved in the USA, Europe and/ or Japan for RA treatment. Evidence from the literature indicates that JAK inhibitors interfere with B cell functions. In this review, the main results obtained in clinical trials, pharmacokinetic, in vitro and in vivo studies concerning the effects of JAK inhibitors on B cell immune responses in RA are summarized.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationFront Med (Lausanne). 2021 Feb 5;7:607725.pt_PT
dc.identifier.doi10.3389/fmed.2020.607725pt_PT
dc.identifier.eissn2296-858X
dc.identifier.urihttp://hdl.handle.net/10451/46766
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherFrontierspt_PT
dc.relation.publisherversionhttps://www.frontiersin.org/journals/medicine#pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectB cellspt_PT
dc.subjectJAK inhibitorspt_PT
dc.subjectJAK-STAT pathwaypt_PT
dc.subjectCytokinespt_PT
dc.subjectRheumatoid arthritispt_PT
dc.titleJAK inhibitors and modulation of B cell immune responses in rheumatoid arthritispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.titleFrontiers in Medicinept_PT
oaire.citation.volume7pt_PT
person.familyNameMoura
person.familyNameFonseca
person.givenNameRita
person.givenNameJoão
person.identifier503714
person.identifier.ciencia-idF21E-178E-DB12
person.identifier.ciencia-idF310-B85D-57C7
person.identifier.orcid0000-0002-9685-6924
person.identifier.orcid0000-0003-1432-3671
person.identifier.scopus-author-id23480391100
person.identifier.scopus-author-id7101983519
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationbb85191e-1ba5-4c49-8677-6f5f8c6fd5b5
relation.isAuthorOfPublication1772dc12-7c55-4c76-ae2d-c23270172480
relation.isAuthorOfPublication.latestForDiscovery1772dc12-7c55-4c76-ae2d-c23270172480

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