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Bystander activation and autoimmunity

dc.creatorPacheco Y.spa
dc.creatorAcosta Ampudia, Yeny Yasbleidyspa
dc.creatorMonsalve Carmona, Diana Marcelaspa
dc.creatorChang C.spa
dc.creatorGershwin M.E.spa
dc.creatorAnaya, Juan-Manuelspa
dc.date.accessioned2020-05-25T23:55:52Z
dc.date.available2020-05-25T23:55:52Z
dc.date.created2019spa
dc.description.abstractThe interaction over time of genetic, epigenetic and environmental factors (i.e., autoimmune ecology) increases or decreases the liability an individual would have to develop an autoimmune disease (AD) depending on the misbalance between risk and protective effects. Pathogens have been the most common antecedent events studied, but multiple other environmental factors including xenobiotic chemicals, drugs, vaccines, and nutritional factors have been implicated into the development of ADs. Three main mechanisms have been offered to explain the development of autoimmunity: molecular mimicry, epitope spreading, and bystander activation. The latter is characterized by auto-reactive B and T cells that undergo activation in an antigen-independent manner, influencing the development and course of autoimmunity. Activation occurs due to a combination of an inflammatory milieu, co-signaling ligands, and interactions with neighboring cells. In this review, we will discuss the studies performed seeking to define the role of bystander activation in systemic and organ-specific ADs. In all cases, we are cognizant of individual differences between hosts and the variable latency time for clinical expression of disease, all of which have made our understanding of the etiology of loss of immune tolerance difficult and enigmatic. © 2019 Elsevier Ltdeng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1016/j.jaut.2019.06.012
dc.identifier.issn10959157
dc.identifier.issn08968411
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/22244
dc.language.isoengspa
dc.publisherAcademic Pressspa
dc.relation.citationTitleJournal of Autoimmunity
dc.relation.citationVolumeVol. 103
dc.relation.ispartofJournal of Autoimmunity, ISSN:10959157, 08968411, Vol.103,(2019)spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85068962845&doi=10.1016%2fj.jaut.2019.06.012&partnerID=40&md5=bbc25d0c85d6fd66f4700282f3709375spa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordAutoimmune diseasespa
dc.subject.keywordAutoimmune hepatitisspa
dc.subject.keywordAutoimmune thyroiditisspa
dc.subject.keywordAutoimmunityspa
dc.subject.keywordBacterial infectionspa
dc.subject.keywordBacteriumspa
dc.subject.keywordBystander effectspa
dc.subject.keywordCell communicationspa
dc.subject.keywordGap junctionspa
dc.subject.keywordGraves diseasespa
dc.subject.keywordHashimoto diseasespa
dc.subject.keywordHostspa
dc.subject.keywordHumanspa
dc.subject.keywordImmunological tolerancespa
dc.subject.keywordInsulin dependent diabetes mellitusspa
dc.subject.keywordLatent periodspa
dc.subject.keywordLegionella pneumophilaspa
dc.subject.keywordMediatorspa
dc.subject.keywordMemory t lymphocytespa
dc.subject.keywordMultiple sclerosisspa
dc.subject.keywordNonhumanspa
dc.subject.keywordParasitosisspa
dc.subject.keywordPriority journalspa
dc.subject.keywordReviewspa
dc.subject.keywordRheumatoid arthritisspa
dc.subject.keywordSystemic lupus erythematosusspa
dc.subject.keywordT lymphocyte activationspa
dc.subject.keywordVaccinationspa
dc.subject.keywordVirus infectionspa
dc.subject.keywordAuto-reactive t cellsspa
dc.subject.keywordAutoimmune diseasesspa
dc.subject.keywordBystander activationspa
dc.subject.keywordCytokinesspa
dc.subject.keywordInfectionspa
dc.subject.keywordT-cell activationspa
dc.titleBystander activation and autoimmunityspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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