Background & Premises: Celiac disease (CD) is an auto-immune enteropathy triggered by ingestion of gluten. Gliadin, a component of the grain protein gluten, is known to induce increased intestinal permeability, which is considered an early crucial biological event in the pathogenesis of CD. Zonulin induces tight junction disassembly. It is therefore considered to be involved in CD. In CD: An increased and persistant release of zonulin and a significant increase in intestinal permeability (S. Drago et al. Scand J Gastroenterol. 2006); Apical, but not basolateral, exposure to gliadin led to zonulin release (MG Clemente et al. Gut 2003). We recently identified the chemokine receptor CXCR3 as the receptor to which gliadin binds. Aim: to explore the function of CXCR3 after gliadin binding