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Molecular mimicry and autoimmunity

dc.creatorAnaya, Juan-Manuel
dc.creatorRestrepo Jimenez, Paulaspa
dc.creatorRojas Quintana, Manuel Eduardospa
dc.creatorPacheco Nieva, Yovana
dc.creatorMonsalve Carmona, Diana Marcela
dc.creatorRamírez Santana, Heily Carolinaspa
dc.date.accessioned2020-08-28T15:48:09Z
dc.date.available2020-08-28T15:48:09Z
dc.date.created2018spa
dc.description.abstractMolecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible individual. However, molecular mimicry is unlikely to be the only underlying mechanism for autoimmune responses; other factors such as breach in central tolerance, non-specific bystander activation, or persistent antigenic stimuli (amongst others) may also contribute to the development of autoimmune diseases. Host genetics, exposure to microbiota and environmental chemicals are additional links to our understanding of molecular mimicry. Our current knowledge of the detailed mechanisms of molecular mimicry is limited by the issues of prolonged periods of latency before the appearance of disease, the lack of enough statistical power in epidemiological studies, the limitations of the potential role of genetics in human studies, the relevance of inbred murine models to the diverse human population and especially the limited technology to systematically dissect the human T-cell repertoire and B-cell responses. Nevertheless, studies on the role of autoreactive T-cells that are generated secondary to molecular mimicry, the diversity of the T-cell receptor repertoires of auto-reactive T-cells, the role of exposure to cryptic antigens, the generation of autoimmune B-cell responses, the interaction of microbiota and chemical adjuvants with the host immune systems all provide clues in advancing our understanding of the molecular mechanisms involved in the evolving concept of molecular mimicry and also may potentially aid in the prevention and treatment of autoimmune diseases.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1016/j.jaut.2018.10.012
dc.identifier.issnISSN:0896-8411
dc.identifier.issnEISSN: 1095-9157
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/28418
dc.language.isoengspa
dc.publisherElsevierspa
dc.relation.citationEndPage123
dc.relation.citationStartPage100
dc.relation.citationTitleJournal of Autoimmunity
dc.relation.citationVolumeVol. 95
dc.relation.ispartofJournal of Autoimmunity, ISSN:0896-8411; EISSN: 1095-9157,Vol. 95 (December 2018); pp. 100-123spa
dc.relation.urihttps://www.sciencedirect.com/science/article/pii/S0896841118305365spa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.sourceJournal of Autoimmunityspa
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR
dc.subject.keywordAutoimmune diseasesspa
dc.subject.keywordAutoimmunityspa
dc.subject.keywordMolecular mimicryspa
dc.subject.keywordCross-reactivityspa
dc.subject.keywordCross reactionsspa
dc.titleMolecular mimicry and autoimmunityspa
dc.title.TranslatedTitleMimetismo molecular y autoinmunidadspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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