i s i t a g [ c t r p Coeliac disease (Cd) is a gluten-sensitive enteropathy of he proximal small intestine, affecting up to 1% of Westrn, North African, Near and Middle Eastern populations 1]. Gluten comprises the storage proteins of wheat, i.e., liadins and glutenins that are present as numerous distinct roteins in each wheat variant [2]. Wheat gliadins and the omologous storage proteins of barley (hordeins) and rye secalins) are the triggers of Cd. Recently, also some of the tructurally distinct glutenin proteins of wheat have been hown to induce an inflammatory T cell response in Cd 3]. Inflammation in Cd is highly variable, with varying egrees of villous atrophy and crypt hyperplasia, and n increase in intraepithelial lymphocytes. Likewise, the ymptoms of Cd patients differ widely, ranging from symptomatic, to atypical or to classical malabsorptive sympoms, characterized by diarrhoea and nutrient deficiencies 4,5]. Manifestation of Cd is genetically determined, requiring he presence of the human leukocyte antigen (HLA) class I molecules DQ2 or DQ8 as necessary precondition. Thus –12% of first degree relatives are also affected by Cd and a oncordance rate of 0.75 was reported among monozygotic wins [6,7]. However, DQ2 or DQ8 are found in 25–40% f the general populations in which Cd occurs, pointing to ther yet largely elusive genetic and acquired factors that rigger the disease [6]. Recently, the DQ2 gene dose has been dentified as one contributory factor, with a higher risk of Q2 homozygotes versus DQ2 heterozygotes to develop Cd 8].