Celiac disease (CD) is an autoimmune disorder characterized by permanent intolerance to dietary gluten resulting in villous atrophy, inflammation and crypt cell hyperplasia in the proximal small intestine. Although some CD patients may suffer primarily from gastrointestinal symptoms, CD may be connected with extra intestinal disorders. Genetic, environmental and immunological factors have been described as responsible for the disease. With the regard of the participation of the immunological system, CD has been correlated with a Th1-like cytokine production profile with particular involvement of Interferon-Î³ (IFN-Î³) and interleukin-18 (IL-18). It has been suggested a role of IFN-Î³ gene polymorphisms in CD susceptibility. Moreover, it has been supposed that haplotypes of the promoter region of IL-18 may contribute to CD risk. It has been reported a higher rate of unresponsiveness to Hepatitis B virus (HBV) vaccine series in CD patients than in healthy controls. Interestingly, Th1cytokines gene polymorphisms have also been seen in association with non responders to the HBV vaccine. Concordantly, it has been written that genetically determined differences in IFN-Î³ activity could impact on the magnitude of immune response to HBV vaccination. In addition, it has been shown a link between IFN-Î³ gene polymorphism and susceptibility to development of intrauterine HBV infection.
Celiac Disease, Hepatitis B Vaccine Nonresponse and Endometriosis: What is the Link?: Raffaella Mormile and Giorgio Vittori
Last date updated on July, 2014