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dc.creatorPacheco Y. 
dc.creatorAcosta-Ampudia, Yeny 
dc.creatorMonsalve, Diana M. 
dc.creatorChang C. 
dc.creatorGershwin M.E. 
dc.creatorAnaya, Juan-Manuel 
dc.date.accessioned2020-05-25T23:55:52Z
dc.date.available2020-05-25T23:55:52Z
dc.date.created2019
dc.identifier.issn10959157
dc.identifier.issn08968411
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/22244
dc.description.abstract"The 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 Ltd"
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.relation.ispartofJournal of Autoimmunity, ISSN:10959157, 08968411, Vol.103,(2019)
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=bbc25d0c85d6fd66f4700282f3709375
dc.sourceinstname:Universidad del Rosario
dc.sourcereponame:Repositorio Institucional EdocUR
dc.titleBystander activation and autoimmunity
dc.typearticle
dc.publisherAcademic Press
dc.subject.keywordAutoimmune disease
dc.subject.keywordAutoimmune hepatitis
dc.subject.keywordAutoimmune thyroiditis
dc.subject.keywordAutoimmunity
dc.subject.keywordBacterial infection
dc.subject.keywordBacterium
dc.subject.keywordBystander effect
dc.subject.keywordCell communication
dc.subject.keywordGap junction
dc.subject.keywordGraves disease
dc.subject.keywordHashimoto disease
dc.subject.keywordHost
dc.subject.keywordHuman
dc.subject.keywordImmunological tolerance
dc.subject.keywordInsulin dependent diabetes mellitus
dc.subject.keywordLatent period
dc.subject.keywordLegionella pneumophila
dc.subject.keywordMediator
dc.subject.keywordMemory t lymphocyte
dc.subject.keywordMultiple sclerosis
dc.subject.keywordNonhuman
dc.subject.keywordParasitosis
dc.subject.keywordPriority journal
dc.subject.keywordReview
dc.subject.keywordRheumatoid arthritis
dc.subject.keywordSystemic lupus erythematosus
dc.subject.keywordT lymphocyte activation
dc.subject.keywordVaccination
dc.subject.keywordVirus infection
dc.subject.keywordAuto-reactive t cells
dc.subject.keywordAutoimmune diseases
dc.subject.keywordBystander activation
dc.subject.keywordCytokines
dc.subject.keywordInfection
dc.subject.keywordT-cell activation
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.type.spaArtículo
dc.rights.accesoAbierto (Texto Completo)
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.identifier.doihttps://doi.org/10.1016/j.jaut.2019.06.012
dc.relation.citationTitleJournal of Autoimmunity
dc.relation.citationVolumeVol. 103


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