Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011;24(3):164-172.

Inflammatory bowel disease: recent advances on genetics and innate immunity

Affiliations
Review

Inflammatory bowel disease: recent advances on genetics and innate immunity

Theodoros Karantanos et al. Ann Gastroenterol. 2011.

Abstract

The chronic inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, are recognized as important causes of gastrointestinal disease in children and adults. Insight into IBD is advancing rapidly owing to a plethora of investigations into intestinal inflammation in animal models, advances in the interrogation of diseases inherited as complex genetic traits, and the development of methods to define the composition of the intestinal microbiota. These advances offer a better understanding of the genetically determined interplay between the commensal microbiota, intestinal cells and the immune system, and the manner in which this interaction might be modified by environmental factors in the pathogenesis of IBD. The present review highlights recent advances in IBD research.

Keywords: IBD; NOD2; autophagy; genetic susceptibility; innate immunity.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest: None

Figures

Figure 1
Figure 1
Factors implicated in the pathophysiology of inflammatory bowel disease (IBD).
Figure 2
Figure 2
The interactions between NOD2 and bacterially induced autophagy mediators in a macrophage upon intracellular infection.
Figure 3
Figure 3
The intracellular consequences of endoplasmic reticulum (ER) stress.

References

    1. Sadlack B, Merz H, Schorle H, Schimpl A, Feller AC, Horak I. Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene. Cell. 1993;75:253–261. - PubMed
    1. Gregersen PK, Olsson LM. Recent advances in the genetics of autoimmune disease. Annu Rev Immunol. 2009;27:363–391. - PMC - PubMed
    1. Peterson DA, Frank DN, Pace NR, Gordon JI. Metagenomic approaches for defining the pathogenesis of inflammatory bowel diseases. Cell Host Microbe. 2008;3:417–427. - PMC - PubMed
    1. Greenstein RJ. Is Crohn's disease caused by a mycobacterium? Comparisons with leprosy, tuberculosis and Johne's disease. Lancet Infect Dis. 2003;3:507–514. - PubMed
    1. Halme L, Paavola-Sakki P, Turunen U, Lappalainen M, Farkkila M, Kontula K. Family and twin studies in inflammatory bowel disease. World J Gastroenterol. 2006;12:3668–3672. - PMC - PubMed

LinkOut - more resources