New knowledge of the pathogenesis of Crohn’s disease

Czech version

Authors: B. Ambrůzová ¹; M. Rédováihash2 ^{1,2,3 1,2,3}
Authors‘ workplace: Advanced Cell Immunotherapy Unit, Lékařská fakulta MU Brno, vedoucí doc. MUDr. Dalibor Valík, Ph. D. ¹; Klinika komplexní onkologické péče, MOÚ Brno, přednosta prof. MUDr. Rostislav Vyzula, CSc. ²; Výzkumná skupina Molekulární onkologie II – solidní nádory Středoevropského technologického institutu Brno, vedoucí RNDr. Ondřej Slabý, Ph. D. ³; Gastroenterologické oddělení, MOÚ Brno, vedoucí MUDr. Milana Šachlová, CSc. et Ph. D. ⁴
Published in: Vnitř Lék 2012; 58(4): 291-298
Category: Reviews

Overview

Crohn’s disease is a complex chronic inflammatory disease of the gastrointestinal tract with multifactorial pathogenesis. Over the recent years, there has been rather a sharp increase in the incidence of Crohn’s disease and, even though this disease had been known for some time, the cause remains unknown. Studies exploring genetic basis of Crohn’s disease have provided new knowledge of the pathogenesis of this disease, suggesting that this may be associated with a failure of mechanisms behind symbiosis of gut microflora and intestinal mucosal immune system. Crohn’s disease seems to be caused by inadequate immune response to intestinal flora in genetically predisposed individuals. Crohn’s disease has been linked to a number of genes. Many of them are related to the modulation of non-specific immune response, defects of which are considered to be key in Crohn’s disease pathogenesis. The aim of this review paper is to summarize the new knowledge on the pathogenesis of Crohn’s disease at the level of polymorphisms of the NOD2, ATG16L1 genes and the IL23-Th17-lymfocytes signalling pathway genes and to consider further research directions in this disease.

Key words:
Crohn’s disease – pathogenesis – NOD2 – ATG16L1 – IL23-Th17-lymphocytes

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