Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2005;43(7):685-95.
doi: 10.1515/CCLM.2005.117.

"Coelionomics": Towards Understanding the Molecular Pathology of Coeliac Disease

Affiliations
Review

"Coelionomics": Towards Understanding the Molecular Pathology of Coeliac Disease

Begoña Diosdado et al. Clin Chem Lab Med. .

Abstract

Coeliac disease (CD) is an inflammatory disorder of the small intestine characterised by a permanent intolerance to gluten-derived peptides. When gluten-derived peptides reach the lamina propria in CD patients, they provoke specific changes in the mucosa of their small intestine. Although the susceptibility to CD is strongly determined by environmental gluten, it is clearly a common genetic disorder. Important genetic factors for CD are the HLA-DQ genes located in the MHC region on chromosome 6 [HLA-DQ2 (95%) or HLA-DQ8 ( approximately 5%) heterodimers]. So far, the only treatment for CD consists of a life-long gluten-free diet. A key question in CD is why the gluten-derived peptides are resistant to further breakdown by endogenous proteases and how, in turn, they can activate a harmful immune response in the lamina propria of genetically predisposed individuals. Four mechanisms, namely apoptosis, oxidative stress, matrix metalloproteinases and dysregulation of proliferation and differentiation, are thought to play a role in the pathophysiology of CD. Whether the genes involved in these four mechanisms play a causative role in the development of the villous atrophy or are, in fact, a consequence of the disease process is unknown. In this review we summarise these mechanisms and discuss their validity in the context of current insights derived from genetic, genomic and molecular studies. We also discuss future directions for research and the therapeutic implications for patients.

Similar articles

See all similar articles

Cited by 15 articles

  • Immune Response to Rotavirus and Gluten Sensitivity.
    Puccetti A, Saverino D, Opri R, Gabrielli O, Zanoni G, Pelosi A, Fiore PF, Moretta F, Lunardi C, Dolcino M. Puccetti A, et al. J Immunol Res. 2018 Mar 15;2018:9419204. doi: 10.1155/2018/9419204. eCollection 2018. J Immunol Res. 2018. PMID: 29736406 Free PMC article.
  • Thiol/disulphide homeostasis in celiac disease.
    Kaplan M, Ates I, Yuksel M, Ozderin Ozin Y, Alisik M, Erel O, Kayacetin E. Kaplan M, et al. World J Gastrointest Pharmacol Ther. 2017 May 6;8(2):120-126. doi: 10.4292/wjgpt.v8.i2.120. World J Gastrointest Pharmacol Ther. 2017. PMID: 28533921 Free PMC article.
  • Protein-protein interaction network of celiac disease.
    Zamanian Azodi M, Peyvandi H, Rostami-Nejad M, Safaei A, Rostami K, Vafaee R, Heidari M, Hosseini M, Zali MR. Zamanian Azodi M, et al. Gastroenterol Hepatol Bed Bench. 2016 Fall;9(4):268-277. Gastroenterol Hepatol Bed Bench. 2016. PMID: 27895852 Free PMC article.
  • Laboratory Medicine in the Scope of Proteomics and Genomics.
    Demkow U. Demkow U. EJIFCC. 2010 Oct 29;21(3):56-63. eCollection 2010 Oct. EJIFCC. 2010. PMID: 27683374 Free PMC article.
  • Bread and Other Edible Agents of Mental Disease.
    Bressan P, Kramer P. Bressan P, et al. Front Hum Neurosci. 2016 Mar 29;10:130. doi: 10.3389/fnhum.2016.00130. eCollection 2016. Front Hum Neurosci. 2016. PMID: 27065833 Free PMC article. Review.
See all "Cited by" articles

Publication types

Substances

Associated data

Feedback