We comprehensively evaluated the expression of therapeutically targetable immune checkpoint molecules involved in celiac disease (CD). We have focused on the alteration of the CD200/CD200R pathway and Elafin expression in celiac disease and discussed their roles in regulating the immune response. There are limited data related to the expression or function of these molecules in celiac disease.
View Article and Find Full Text PDFBackground: We have focused on the alteration of the PD-1/PD-L1 pathway in celiac disease and discussed the roles of the PD1 pathway in regulating the immune response. We explored the idea that the altered mRNA splicing process in key regulatory proteins could represent a novel source to identify diagnostic, prognostic, and therapeutic targets in celiac disease.
Methods: We characterized the PD1 mRNA variants' profile in CD patients and in response to gluten peptides' incubation after experiments.
Arch Immunol Ther Exp (Warsz)
December 2018
Celiac disease is an autoimmune condition triggered by the ingestion of gluten, the protein fraction of wheat, barley and rye. It is not simply an intestinal disease; it is multifactorial caused by many different genetic factors acting together with non-genetic causes. Similar to other autoimmune diseases, celiac disease is a polygenic disorder for which the major histocompatibility complex locus is the most important genetic factor, and is the result of an immune response to self-antigens leading to tissue destruction and the autoantibodies production.
View Article and Find Full Text PDF