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Luke Jostins¹, Stephan Ripke, Rinse K Weersma

¹Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1HH, UK.

|November 7, 2012

Resumen

Este estudio identificó 71 nuevas asociaciones genéticas para la enfermedad inflamatoria intestinal (EII), lo que eleva el total a 163 loci. de EII. Muchos de estos loci se comparten con otros trastornos inmunes y respuestas a las infecciones micobacterianas.

Área de la Ciencia:

Genética La genética.
Inmunología Inmunología.
Gastroenterología y Gastroenterología.

Sus antecedentes:

La enfermedad inflamatoria intestinal (EII), que abarca la enfermedad de Crohn y la colitis ulcerosa, afecta a millones de personas en todo el mundo.
Estudios previos de asociación genómica (GWAS) han implicado nuevas vías como la autofagia en la patogénesis de la EII.
Algunos loci de susceptibilidad a la EII se comparten con otras afecciones inflamatorias.

Objetivo del estudio:

Ampliar el conocimiento de las vías relacionadas con la EII a través de un metanálisis a gran escala.
Identificar nuevos loci genéticos asociados con la enfermedad de Crohn y la colitis ulcerosa.
Para investigar la superposición de los loci de la EII con otros trastornos e infecciones inmunomediados.

Principales métodos:

Metaanálisis de los datos de GWAS de más de 75.000 casos y controles para la enfermedad de Crohn y la colitis ulcerosa.
Validación extensa de hallazgos genéticos significativos.
Análisis de redes de coexpresión génica para explorar las relaciones de las vías.

Principales resultados:

Identificación de 71 nuevos loci asociados a la EII, lo que eleva el total a 163 loci significativos en todo el genoma.
La mayoría de los loci identificados están asociados tanto con la enfermedad de Crohn como con la colitis ulcerosa.
Se observó una superposición significativa entre los loci de la EII y los de la espondilitis anquilosante, la psoriasis y la susceptibilidad a las infecciones micobacterianas.

Conclusiones:

El estudio amplía significativamente el número de loci genéticos conocidos de EII.
La patogénesis de la EII involucra factores genéticos compartidos con otras enfermedades inmunomediadas y respuestas del huésped a las micobacterias.
La evidencia de la selección tanto direccional como de equilibrio que actúa sobre los loci de la EII sugiere presiones evolutivas complejas.

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