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dc.creatorAnaya, Juan-Manuel 
dc.date.accessioned2020-05-07T15:04:14Z
dc.date.available2020-05-07T15:04:14Z
dc.date.created2010
dc.date.issued2010
dc.identifier.issn1478-6354
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/21895
dc.description.abstractAlthough autoimmune diseases exhibit contrasting epidemiological features, pathology, and clinical manifestations, three lines of evidence demonstrate that these diseases share similar immunogenetic mechanisms (that is, autoimmune tautology). First, clinical evidence highlights the co-occurrence of distinct autoimmune diseases within an individual (that is, polyautoimmunity) and within members of a nuclear family (that is, familial autoimmunity). Second, physiopathologic evidence indicates that the pathologic mechanisms may be similar among autoimmune diseases. Lastly, genetic evidence shows that autoimmune phenotypes might represent pleiotropic outcomes of the interaction of non-specific disease genes. © 2010 BioMed Central Ltd.
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.relation.ispartofArthritis Research and Therapy, ISSN: 1478-6354 Vol. 12, No. 6 (2010)
dc.relation.urihttps://arthritis-research.biomedcentral.com/track/pdf/10.1186/ar3175
dc.subject.ddcEnfermedades 
dc.titleThe autoimmune tautology
dc.typeother
dc.subject.keywordAutoimmunity
dc.subject.keywordEditorial
dc.subject.keywordGenetic risk
dc.subject.keywordGenetic susceptibility
dc.subject.keywordImmunogenetics
dc.subject.keywordAutoimmune disease
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.type.spaEditorial
dc.rights.accesoAbierto (Texto Completo)
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.creator.googleAnaya, Juan-Manuel
dc.identifier.doihttps://doi.org/10.1186/ar3175
dc.relation.citationIssueNo. 6
dc.relation.citationTitleArthritis Research and Therapy
dc.relation.citationVolumeVol. 12
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR


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