CELL-MEDIATED IMMUNITY TO GLIADIN WITHIN THE SMALL-INTESTINAL MUCOSA IN CELIAC DISEASE

2009 ◽  
Vol 33 (9) ◽  
pp. 267-268
2021 ◽  
Vol 9 (3) ◽  
pp. 547
Author(s):  
Daniel Sánchez ◽  
Iva Hoffmanová ◽  
Adéla Szczepanková ◽  
Věra Hábová ◽  
Helena Tlaskalová-Hogenová

The ingestion of wheat gliadin (alcohol-soluble proteins, an integral part of wheat gluten) and related proteins induce, in genetically predisposed individuals, celiac disease (CD), which is characterized by immune-mediated impairment of the small intestinal mucosa. The lifelong omission of gluten and related grain proteins, i.e., a gluten-free diet (GFD), is at present the only therapy for CD. Although a GFD usually reduces CD symptoms, it does not entirely restore the small intestinal mucosa to a fully healthy state. Recently, the participation of microbial components in pathogenetic mechanisms of celiac disease was suggested. The present review provides information on infectious diseases associated with CD and the putative role of infections in CD development. Moreover, the involvement of the microbiota as a factor contributing to pathological changes in the intestine is discussed. Attention is paid to the mechanisms by which microbes and their components affect mucosal immunity, including tolerance to food antigens. Modulation of microbiota composition and function and the potential beneficial effects of probiotics in celiac disease are discussed.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Natalia M. Bottasso Arias ◽  
Marina García ◽  
Constanza Bondar ◽  
Luciana Guzman ◽  
Agustina Redondo ◽  
...  

Celiac disease (CD) is an immune-mediated enteropathy that develops in genetically susceptible individuals following exposure to dietary gluten. Severe changes at the intestinal mucosa observed in untreated CD patients are linked to changes in the level and in the pattern of expression of different genes. Fully differentiated epithelial cells express two isoforms of fatty acid binding proteins (FABPs): intestinal and liver, IFABP and LFABP, respectively. These proteins bind and transport long chain fatty acids and also have other important biological roles in signaling pathways, particularly those related to PPARγand inflammatory processes. Herein, we analyze the serum levels of IFABP and characterize the expression of both FABPs at protein and mRNA level in small intestinal mucosa in severe enteropathy and normal tissue. As a result, we observed higher levels of circulating IFABP in untreated CD patients compared with controls and patients on gluten-free diet. In duodenal mucosa a differential FABPs expression pattern was observed with a reduction in mRNA levels compared to controls explained by the epithelium loss in severe enteropathy. In conclusion, we report changes in FABPs’ expression pattern in severe enteropathy. Consequently, there might be alterations in lipid metabolism and the inflammatory process in the small intestinal mucosa.


2000 ◽  
Vol 118 (4) ◽  
pp. A369
Author(s):  
Ian Perry ◽  
Chris Tselepis ◽  
D Scott A. Sanders ◽  
Janusz A. Jankowski ◽  
Brian T. Cooper ◽  
...  

1989 ◽  
Vol 26 (3) ◽  
pp. 273-273 ◽  
Author(s):  
J Schweizer ◽  
H L Mearin ◽  
A S Pena ◽  
G J A Offerhaus ◽  
E J Dreef ◽  
...  

Author(s):  
Majid Aflatoonian

Introduction: Celiac disease is an autoimmune disease caused by persistent intolerance to gluten, which is causedin people who are genetically predisposed.The disease presents with atrophy of the small intestinal mucosa and gastrointestinal and extra-gastrointestinal manifestations.Environmental factors like gluten and genetic factors such as HLA and non-HLA genes are involved in causing the disease.Mucosal atrophy results from an adaptive and innate immune response to gluten. T-helper, interleukin 15 and tumor necrosisfactor-alpha have a central role in this process. Recognize the risk of genetic factors and inflammatorymechanisms will help diagnose and treat the disease.


2012 ◽  
Vol 54 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marko Kalliomäki ◽  
Reetta Satokari ◽  
Hannu Lähteenoja ◽  
Sanna Vähämiko ◽  
Juhani Grönlund ◽  
...  

1992 ◽  
Vol 14 (2) ◽  
pp. 173-176 ◽  
Author(s):  
D. Branski ◽  
H. Hurvitz ◽  
A. Halevi ◽  
A. Klar ◽  
P. Navon ◽  
...  

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