Background: Enteropathy in coeliac disease (CD) is sustained by a gliadin specific Th1 response. Interleukin (IL)-10 can downregulate Th1 immune responses. Aim: We investigated the ability of recombinant human (rh) IL-10 to suppress gliadin induced Th1 response. Patients and methods: IL-10 RNA transcripts were analysed by competitive reverse transcription polymerase chain reaction in duodenal biopsies from untreated and treated CD patients, non-coeliac enteropathies (NCE), and controls. CD biopsies were cultured with a peptic-tryptic digest of gliadin with or without rhIL-10. The proportion of CD80+and CD25+cells in the lamina propria, epithelial expression of Fas, intraepithelial infiltration of CD3+cells, as well as cytokine synthesis (Interferon γ.(IFN-γ) and IL-2) were measured. Short term T cell lines (TCLs) obtained from treated CD biopsies cultured with gliadin with or without rhIL-10 were analysed by ELISPOT for gliadin specific production of IFN-γ. Results: In untreated CD and NCE, IL-10 RNA transcripts were significantly upregulated. In ex vivo organ cultures, rhIL10 downregulated gliadin induced cytokine synthesis, inhibited intraepithelial migration of CD3+cells, and reduced the proportion of lamina propria CD25+and CD80+cells whereas it did not interfere with epithelial Fas expression. In short term TCLs, rhIL-10 abrogated the IFN-γresponse to gliadin. Conclusions: rhIL-10 suppresses gliadin specific T cell activation. It may interfere with the antigen presenting capacity of lamina propria mononuclear cells as it reduces the expression of CD80. Interestingly, rhIL-10 also induces a long term hyporesponsiveness of gliadin specific mucosal T cells. These results offer new perspectives for therapeutic strategies in coeliac patients based on immune modulation by IL-10. Background: Enteropathy in coeliac disease (CD) is sustained by a gliadin specific Th1 response. Interleukin (IL) -10 can downregulate Th1 immune responses. Aim: We investigated the ability of recombinant human (rh) IL- response. Patients and methods: IL-10 RNA transcripts were analysed by competitive reverse transcription polymerase chain reaction in duodenal biopsies from untreated and treated CD patients, non-coeliac enteropathies (NCE), and controls. CD biopsies were cultured with a peptic-tryptic digest of gliadin with or without rhIL-10. The proportions of CD80 + and CD25 + cells in the lamina propria, epithelial expression of Fas, intraepithelial infiltration of CD3 + cells, as well as cytokine synthesis (Interferon gamma. Short term T cell lines (TCLs) obtained from treated CD biopsies cultured with gliadin with or without rhIL-10 were analyzed by ELISPOT for gliadin specific production of IFN-γ. Results: In untreated CD In ex vivo organ cultures, rhIL10 downregulated gliadin induced cytokine synthesis, inhibited intraepithelial migration of CD3 + cells, and reduced the proportion of lamina propria CD25 + and CD80 + cells but it did not not interfere with epithelial Fas expression. In short term TCLs, rhIL-10 abrogated the IFN-γresponse to gliadin. Conclusions: rhIL-10 suppresses gliadin specific T cell activation. It may interfere with the antigen presenting capacity of lamina propria mononuclear cells as it reduces the expression of CD80. Interestingly, rhIL-10 also induces a long term hyporesponsiveness of gliadin specific mucosal T cells. These results offer new perspectives for therapeutic strategies in coeliac patients based on immune modulation by IL-10.