MICA response to gliadin in intestinal mucosa from celiac patients View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-10-14

AUTHORS

Ainhoa Martín-Pagola, Gustavo Pérez-Nanclares, Lourdes Ortiz, Juan Carlos Vitoria, Idoia Hualde, Rosa Zaballa, Enriqueta Preciado, Luis Castaño, J. Ramón Bilbao

ABSTRACT

MHC class I chain-related gene A (MICA), a putative independent susceptibility gene in autoimmune diseases, encodes a surface protein present in epithelial cells that binds to NKG2D, an activating receptor of NK, αβ and γδ T cells, and could function as a stress-inducible activator of the innate immune response. There is no evidence of a long-term implication of MICA in the celiac autoimmune process. However, it could be that gliadin activation of MICA occurs only during the initial stages of the disease. In order to determine whether MICA is activated in response to gliadin in patients with celiac disease (CD), small intestinal mucosa biopsy samples from ten long-standing celiac patients on a gluten-free diet and from five non-celiac individuals were incubated with and without gliadin for 4 h. Total RNA was purified and MICA, IFNG and NKG2D mRNA were quantified by fluorescent real-time RT-PCR. Expression levels were calculated relative to GAPDH. MICA expression was detected in both patients and controls, but incubation with gliadin induced a strong increase in samples from the treated CD group compared with the non-CD controls (P=0.028), while no differences were observed for IFNG or NKG2D mRNA levels. The gliadin-provoked over-expression of MICA in “normalized” tissues from CD patients suggests a role for this stress-induced activator of the immune response in the early stages of organ-specific autoimmune destruction, probably preceding the onset of inflammation. More... »

PAGES

549-554

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00251-004-0724-8

DOI

http://dx.doi.org/10.1007/s00251-004-0724-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022363170

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15490153


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