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dc.contributor.authorDíaz-Peña R.
dc.contributor.authorValdés E.
dc.contributor.authorCofré C.
dc.contributor.authorCastro-Santos P.
dc.date.accessioned2020-09-02T22:16:51Z
dc.date.available2020-09-02T22:16:51Z
dc.date.issued2015
dc.identifier.citation107, 9, 560-566
dc.identifier.issn11300108
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4360
dc.descriptionInflammatory bowel disease (IBD) is an entity that mainly includes ulcerative colitis (UC) and Crohn’s disease (CD). Improved health care, diet changes, and higher industrialization are associated with an increase in IBD prevalence. This supports the central role of environmental factors in the pathology of this disease. However, IBD also shows a relevant genetic component as shown by high heritability. Classic genetic studies showed relevant associations between IBD susceptibility and genes involved in the immune response. This is consistent with prior theories about IBD development. According to these, contact of the immune system with a high number of harmless antigens from the diet and the bacterial flora should originate tolerance while preserving response against pathogens. Failure to achieve this balance may originate the typical inflammatory response associated with IBD. Recently, genome-wide association studies (GWASs) have confirmed the implication of the immune system, particularly the Th17 immune response, previously associated to other autoimmune diseases, and of autophagy. In this paper, the mechanisms involved in these two relevant pathways and their potential role in the pathogenesis of IBD are reviewed. © 2015 Arán Ediciones, S. L.
dc.language.isoen
dc.language.isoes
dc.publisherARAN Ediciones S.A.
dc.subjectAutophagy
dc.subjectCrohn’s disease
dc.subjectGenome-wide association studies
dc.subjectInflammatory bowel disease
dc.subjectTh17
dc.subjectUlcerative colitis
dc.subjectcaspase recruitment domain protein 15
dc.subjectgranulocyte macrophage colony stimulating factor
dc.subjectinterleukin 10
dc.subjectinterleukin 21
dc.subjectinterleukin 23
dc.subjecttoll like receptor
dc.subjecttransforming growth factor
dc.subjecttumor necrosis factor alpha
dc.subjectautophagy
dc.subjectbacterial flora
dc.subjectcell differentiation
dc.subjectdiet
dc.subjectdisease course
dc.subjectenvironmental factor
dc.subjectgenetic association
dc.subjectgenetic polymorphism
dc.subjectgenetic regulation
dc.subjectgenetic risk
dc.subjectgenetic susceptibility
dc.subjecthealth care
dc.subjectheritability
dc.subjecthuman
dc.subjectimmune response
dc.subjectinflammatory bowel disease
dc.subjectmeta analysis (topic)
dc.subjectprevalence
dc.subjectprotein expression
dc.subjectReview
dc.subjectrisk assessment
dc.subjectsignal transduction
dc.subjectsingle nucleotide polymorphism
dc.subjectTh17 cell
dc.titleTh17 response and autophagy - Main pathways implicated in the development of inflammatory bowel disease by genome-wide association studies: New factors involved in inflammatory bowel disease susceptibility [Respuesta Th17 y autofagia: Principales vías implicadas en enfermedad inflamatoria intestinal por los estudios de asociación de genoma completo: Nuevos factores implicados en la susceptibilidad a enfermedad inflamatoria intestinal]
dc.typeReview


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