The inherited immune sensitivity to ingested gluten in celiac disease is caused by activation of effector CD4+ T cells (T-helper cells) in the lamina propria (tissues underlying the mucosal surface) by peptides derived from gluten protein in wheat, rye, barley and, for some people, oats.
Activation of these immune cells leads to the release of cytokines which play a crucial role in the pathogenesis of celiac disease, controlling many aspects of the inflammatory immune response.1
Cytokine levels are relevant markers of disease activity:
A prominent finding is the release of both T-cell subsets, Th1 (IFN-gamma, IL-2) and Th2 (IL-4, IL-10)-associated cytokine transcripts, in the same biopsies and peripheral blood cells from patients with active celiac disease.
On the contrary, the release of IL-2 and IL-4 was not observed in peripheral blood samples from inactive celiac disease patients.2
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