The coeliac condition (CD) is characterized by partial or total villus atrophy which results in a malabsorption syndrome that affects sugars, fatty acids, monoglycerides, amino acids, water and electrolytes, as a result of gluten ingestion. The T-lymphocytes infiltrate the small intestine and trigger other lymphocytes to produce cytokines, such as interferon-γ , interleukin (IL)–4 and tumour necrosis factor (TNF)-α that induce the pathological changes [1]. A putative coeliac locus has been identified on chromo­some 2q33, in particular the immuno-regulatory CD28/ CTLA4/ICOS gene cluster, whose protein products are involved in T-cell activation and proliferation [2]. We undertook the analysis of two single nucleotide polymor­phisms (SNPs), one at position –318 (C→T) located in the promoter region, and the +49 (A→G) in the first exon of the CTLA4 gene corresponding to a Thr→Ala change in the leader peptide of the gene product.