New insights on the role of T-cels in the pathogenesis of Celiac Disease

Rossella Cianci, Danilo Pagliari, Raffaele Landolfi, Simona Frosali, Amira Colagiovanni, Giovanni Cammarota, Franco Pandolfi

Risultato della ricerca: Contributo in rivistaArticolo in rivista


Despite intense investigation, the pathogenetic mechanisms leading to villous atrophy in Celiac disease (CD) remain not completely understood. The traditional interpretation is that CD4 cells recognize gliadin and develop an inflammatory reaction by production of Th1 cytokines at the mucosa level inducing CD8 cells to kill mucosal cells by a direct cytotoxic mechanism or by Fas-mediated apoptosis. Recent data, however, have shown that novel CD4 T-cells subpopulations, CD4+ CD25+ Regulatory T-cells (Tregs) and Th17 cells also play a role in the ongoing inflammatory process. Both Tregs and Th17 cells are increased in active CD. However, because Tregs have a suppressive activity on inflammation, their role is controversial. In this editorial we discuss these recent findings and the hypothesis formulated to explain the increase of Tregs. To understand the pathogenesis of tissue damage of CD, we have focused on the duodenal micro-environment, introducing the new concept of “immunological niche” that in CD summarizes cellular and cytokine interactions in duodenal mucosa, where a high plasticity of T-cell subsets is present. CD is often complicated by T-cell lymphomas, especially in cases of refractory CD.
Lingua originaleEnglish
pagine (da-a)171-179
Numero di pagine9
Stato di pubblicazionePubblicato - 2012


  • Celiac disease
  • Immunological niche
  • T cells


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