| Literature DB >> 26139981 |
Abstract
Celiac disease (CD) is a T-cell mediated immune disease in which gliadin-derived peptides activate lamina propria effector CD4+ T cells. This activation leads to the release of cytokines, compatible with a Th1-like pattern, which play a crucial role in the pathogenesis of CD, controlling many aspects of the inflammatory immune response. Recent studies have shown that a novel subset of effector T cells, characterized by expression of high levels of IL-17A, termed Th17 cells, plays a pathogenic role in CD. While these effector T cell subsets produce proinflammatory cytokines, which cause substantial tissue injury in vivo in CD, recent studies have suggested the existence of additional CD4(+) T cell subsets with suppressor functions. These subsets include type 1 regulatory T cells and CD25(+)CD4(+) regulatory T cells, expressing the master transcription factor Foxp3, which have important implications for disease progression.Entities:
Keywords: Celiac disease; Th1 cells; Th17 cells; Treg cells
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Year: 2015 PMID: 26139981 PMCID: PMC4481430 DOI: 10.3748/wjg.v21.i24.7349
Source DB: PubMed Journal: World J Gastroenterol ISSN: 1007-9327 Impact factor: 5.742