AI Article Synopsis
- Celiac disease (CD) is an autoimmune disorder caused by gluten intolerance, potentially linked to issues with immune tolerance.
- Researchers compared the number and function of regulatory T-cells (Tregs) in celiac patients and healthy individuals, finding no differences in cell numbers or regulatory marker expression.
- However, the suppressive functionality of Tregs was significantly reduced in celiac patients, indicating that impaired Treg function may contribute to CD and its associated autoimmune conditions.
Article Abstract
Celiac disease (CD) is characterized by intolerance to gluten and high risk of developing autoimmune phenomena. Possible defects in immune tolerance could have a role in the pathogenesis of the disease. As regulatory T-cells (Tregs) are the main population involved in maintaining peripheral tolerance, we investigated the number of these cells in celiac patients as compared with healthy donors. Moreover, we analyzed the suppressive function of CD4+CD25+ T-cells from celiac disease patients and controls on autologous responder T-cells (CD4+CD25-). The percentage of CD4+CD25+FOXP3+ cells was not different in celiacs and in healthy controls, and among positive cells the level of expression of the two regulatory markers was comparable. However, the suppressor activity of Tregs was significantly impaired in CD patients. These results suggest that a defect in Tregs function could play a role in the pathogenesis of CD and in CD-associated autoimmunity.
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| http://dx.doi.org/10.1007/s10620-008-0501-x | DOI Listing |
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