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Abstract
Celiac disease (CD) is an immunological disorder caused by intolerance to ingested gliadin and other cereal prolamins that has been included in the TH1-dominated group of diseases, where IL-12 induced IFNγ is the major proinflamatory signal. Recently, another linage of T cells has been described, namely TH17, characterized by production of IL-17, that differentiate in response to TGFβ and IL-6 and participate in the pathogenesis of several autoimmune diseases. Using RT-PCR analysis of gene expression, we analyzed the presence of TH1 (IL-12 and IFNγ) and TH17 (TGFβ, IL-6, IL-17A, IL-17F and IL-23) related cytokines in intestinal biopsies from CD patients with active disease compared to remission and from treated patients after acute, in vitro re-exposure to gliadin. Potent TH1 and TH17 responses were present in the active stage of the disease, whereas short incubation of normalized biopsies with gliadin did not increase the expression of the effector cytokines, although a tendency of upregulation for both TH1 and TH17 promoting factors was observed, suggestive of a reactivation of proinflammatory pathways. These results place CD into the group of autoimmune disorders in which TH17 cells also participate, although the relative importance of each T cell response and their role in the initial events of the disease need further investigation.
Acknowledgements
This work was partially funded by Research Project grants 06/111030 from the Basque Department of Health and PI07/0796 from the Instituto de Salud Carlos III of the Spanish Ministry of Health and a Research Award from the Celiac Patient Association from Madrid. Ainara Castellanos-Rubio and Izortze Santín are predoctoral fellows supported by grants from the Spanish Ministry of Education and the University of the Basque Country, respectively. Jose Ramon Bilbao is co-funded by the I3SNS Program of the Spanish Ministry of Health (CES05/036).
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.