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
. 2014 Mar 28;20(12):3255-64.
doi: 10.3748/wjg.v20.i12.3255.

Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease

Affiliations
Review

Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease

Xiao-Rong Xu et al. World J Gastroenterol. .

Abstract

Inflammatory bowel disease (IBD) includes Crohn's disease and ulcerative colitis. The exact etiology and pathology of IBD remain unknown. Available evidence suggests that an abnormal immune response against the microorganisms in the intestine is responsible for the disease in genetically susceptible individuals. Dysregulation of immune response in the intestine plays a critical role in the pathogenesis of IBD, involving a wide range of molecules including cytokines. On the other hand, besides T helper (Th) 1 and Th2 cell immune responses, other subsets of T cells, namely Th17 and regulatory T cells, are likely associated with disease progression. Studying the interactions between various constituents of the innate and adaptive immune systems will certainly open new horizons of the knowledge about the immunologic mechanisms in IBD.

Keywords: Crohn’s disease; Inflammatory bowel disease; Proinflammatory cytokines; T helper 17 cells; T helper cells; Ulcerative colitis.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Pathogenesis of inflammatory bowel disease. DC: Dendritic cell; NK: Natural killer; Th: T helper; Treg: T regulator cell; CTL: Cytotoxic T lymphocyte; Mf: Macrophages.
Figure 2
Figure 2
Pleiotropic role of interleukin-21 in immune responses. IFN: Interferon; IL: Interleukin; CD: Crohn’s disease; DC: Dendritic cell; NK: Natural killer; CTL: Cytotoxic T lymphocyte.
Figure 3
Figure 3
Overexpression of interleukin-23 in inflamed mucosa of patients with inflammatory bowel disease weakens the intestinal defensive barrier and disturbs the immune regulation in intestinal mucosa. IEL: Intestinal epithelial lymphocyte; IL: Interleukin; Th: T helper; Treg: T regulator cell; DC: Dendritic cell.
Figure 4
Figure 4
Inhibitory role of interleukin-25 in intestinal mucosa. IEL: Intestinal epithelial lymphocyte; IL: Interleukin; Th: T helper; Treg: T regulator cell; CTL: Cytotoxic T lymphocyte; Mf: Macrophages; IEC: Intestinal epithelial cells; IBD: Inflammatory bowel disease.

References

    1. Baumgart DC, Sandborn WJ. Crohn’s disease. Lancet. 2012;380:1590–1605. - PubMed
    1. Manichanh C, Borruel N, Casellas F, Guarner F. The gut microbiota in IBD. Nat Rev Gastroenterol Hepatol. 2012;9:599–608. - PubMed
    1. Ordás I, Eckmann L, Talamini M, Baumgart DC, Sandborn WJ. Ulcerative colitis. Lancet. 2012;380:1606–1619. - PubMed
    1. Latella G, Papi C. Crucial steps in the natural history of inflammatory bowel disease. World J Gastroenterol. 2012;18:3790–3799. - PMC - PubMed
    1. Liu Z, Yang L, Cui Y, Wang X, Guo C, Huang Z, Kan Q, Liu Z, Liu Y. Il-21 enhances NK cell activation and cytolytic activity and induces Th17 cell differentiation in inflammatory bowel disease. Inflamm Bowel Dis. 2009;15:1133–1144. - PubMed

Publication types

MeSH terms