Immunity y Helicobacter pylori

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dc.catalogadorpau
dc.contributor.authorHarris, Paul R.
dc.date.accessioned2024-01-19T19:22:45Z
dc.date.available2024-01-19T19:22:45Z
dc.date.issued2011
dc.description.abstractHelicobacter pylori a Gram negative bacterium that colonizes gastric mucosa and that has been associated to different disease such as chronic gastritis, duodenal ulcers and gastric cancer. Although the infection by itself is able to produce damage to the gastric mucosa through the expression and interaction of well-known virulence factors, the immune local response is strongly involved in the pathogenesis of H. pylori-associated diseases. The classic dichotomy T helper type 1 vs type 2 response to explain the damage associated to the bacterium, has been reevaluated in a more complex scenario with the recent description of the T regulatory response and the new patterns of T helper response such as Th17. The extremely well balanced equilibrium between virulence and immune infl ammatory response is mainly regulated by the intensity of the T regulatory response; its suppression would allow the expression of different T helper responses that account for the fi nal damage and clinical outcomes.
dc.fechaingreso.objetodigital2024-05-07
dc.fuente.origenORCID-ene24
dc.identifier.doi10.5867/medwave.2011.03.4950
dc.identifier.issn0716-1018
dc.identifier.urihttp://doi.org/10.5867/medwave.2011.03.4950
dc.identifier.urihttps://www.medwave.cl/puestadia/conferencias/4950.html?lang=en
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/80846
dc.information.autorucEscuela de Medicina; Harris Diez, Paul Richard; 0000-0001-6226-0957; 80706
dc.issue.numero2
dc.language.isoes
dc.nota.accesoContenido completo
dc.revistaGastroenterología latinoamericana
dc.rightsacceso abierto
dc.subjectHelicobacter pylories_ES
dc.subjectregulatory T-cellses_ES
dc.subjectT-helper responsees_ES
dc.titleImmunity y Helicobacter pylories_ES
dc.titleImmunity y Helicobacter pylori
dc.typeartículo
dc.volumen21
sipa.codpersvinculados80706
sipa.trazabilidadORCID;2024-01-08
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