The role of Th1 and Th17 in the pathogenesis of celiac disease

Abstract

Celiac disease is a chronic autoimmune disease that is associated with genetic, environmental and immunological factors. The disease is closely associated with genes that code for human leukocyte antigens DQ2 and DQ8 haplotypes. In general, celiac disease has been recognized as a T lymphocyte associated disorders in which proteins derived gliadins, in the form of naive or deamidated by tissue Transglutaminase, activate T lymphocytes and as a result, release proinflammatory cytokines Such as IFNγ, IL-17, IL-21 and etc. These cytokines lead to histopathological changes like villous atrophy and crypt hyperplasia In addition, celiac disease has a specific antibody against gluten and an autoantigen of the transglutaminase 2(TG2) that provides strong opportunities to fully understand the adaptive immune response leading to disease. In this review, we investigated the role of Th1 and Th17 as an important mediators in pathogenesis of celiac disease.

Alterations in the Composition of the Gut Microbiota in Celiac Disease, Non-Coeliac Gluten Sensitivity and Irritable Bowel Syndrome

“…For instance, irritable bowel syndrome (IBS), which is a result of stress and its symptoms including abdominal pain, changes in the bowel movements, can decrease the diversity of the microbiome with low levels of fecal Lactobacilli and Bi dobacteria, high levels of facultative anaerobic bacteria such as Escherichia coli, and increased ratios of Firmicutes to Bacteroidetes [16,17]. In addition, in ammatory responses in coeliac disease (CD) and non-coeliac gluten sensitivity (NCGS) which are caused by interferon-gamma (IFN-γ), interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α) can stimulate the innate immune response and alter the microbiome composition [18][19][20]. These dissimilarities with a healthy microbiome are affective in GI symptoms in these patients [21].…”