Intestinal T-cell Responses in Celiac Disease – Impact of Celiac Disease Associated Bacteria

Dysbiosis Intraepithelial lymphocyte Lamina propria
DOI: 10.1371/journal.pone.0053414 Publication Date: 2013-01-10T00:11:30Z
ABSTRACT
A hallmark of active celiac disease (CD), an inflammatory small-bowel enteropathy caused by permanent intolerance to gluten, is cytokine production intestinal T lymphocytes. Prerequisites for contracting CD are that the individual carries MHC class II alleles HLA-DQ2 and/or HLA-DQ8 and exposed gluten in diet. Dysbiosis resident microbiota has been suggested be another risk factor CD. In fact, rod shaped bacteria adhering small mucosa were frequently seen patients with during “Swedish epidemic” bacterial candidates could later isolated from born epidemic suggesting long-lasting changes gut microbiota. Interleukin-17A (IL-17A) plays a role both inflammation anti-bacterial responses. IL-17A was produced CD8+ cells (Tc17) CD4+ (Th17), intraepithelial Tc17 being dominant producers. Gluten peptides as well associated induced responses ex vivo challenged biopsies inactive The response suppressed when mixture added while reverse case after epidemic. Under these conditions Th17 Thus seem pave way chronic interferon-γ-production Tc1 lamina propria Th1 cells. dysbiosis they might cause may either directly influencing immune or enhancing gluten.
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