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Background  Inflammatory bowel diseases (IBD) are chronic diseases of the gastrointestinal tract. Although their pathogenesis is unclear, the combination of genetic predisposition and environmental components are believed to be the main cause of these diseases. Recently, many variants in interleukin 23 receptor ( IL23R ) and autophagy-related 16-like 1 ( ATG16L1 ) genes have been associated with the disease. Our objective was to assess the frequency of  ATG16L1  (T300A) and  IL23R  (L310P) variants in Moroccan IBD (Crohn’s disease and Ulcerative Colitis) patients and to evaluate a possible effect of these variants on disease’s phenotype and clinical course.    Methods  96 Moroccan IBD patients and 114 unrelated volunteers were genotyped for  ATG16L1  (T300A) and  IL23R  (L310P) variants by PCR-restriction fragment length polymorphism.    Results  This is the first report on the prevalence of  ATG16L1  (T300A) and  IL23R  (L310P) variants in a Moroccan group. We found that  IL23R  (L310P) variant conferred a protective effect for crohn’s disease (CD) but not ulcerative colitis (UC) patients. The presence of  ATG16L1  (T300A) mutated alleles was associated with CD type but not with disease onset. In addition, the carriage of T300A variant alleles conferred a protective effect in UC.    Conclusion  Our results showed that the prevalence of  ATG16L1  and  IL23R  variants was not significantly different between patients and controls. However a possible role of  ATG16L1  (T300A) on CD phenotype was suggested.    Electronic supplementary material  The online version of this article (doi:10.1186/1756-0500-7-570) contains supplementary material, which is available to authorized users.

IL23R and ATG16L1 variants in Moroccan patients with inflammatory bowel disease