Celiac Disease: Genetics, Pathogenesis and Therapy 2.0

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue, “Celiac Disease: Genetics, Pathogenesis and Therapy 2.0”.

Celiac disease is regarded as an autoimmune disorder triggered, in genetically predisposed individuals, by exposure to gluten. Throughout the years, our understanding of celiac disease has changed quite dramatically, and data obtained by several research groups have allowed us to better define the pathogenesis of this multifactorial disorder.

Although it is known that a specific HLA is necessary for the development of the disease, the presence of the DQ2.5 or DQ8 heterodimer is not sufficient; several loci, harboring genes involved in the immune response, have been identified using GWAS, but still about 50% of genetic predisposition is unknown.

Thus, further clarification of the genetic as well as pathogenetic mechanisms is still needed. This could include the evaluation of epigenetic mechanisms, such as DNA methylation, but also of the role of miRNAs and other non-coding RNAs. Further, the interactions between the various gliadin peptides and specific cellular pathways can still provide additional data that could help to further elucidate the mechanisms involved in the generation of intestinal damage. Last but not least, we should consider the role of microbiota, in particular regarding its ability to interact with gluten peptides but also with the intestinal immune system.

The understanding of pathogenetic pathways allows us to identify possible targets for new therapies, among which there could be molecules that are able to prevent gliadin peptide intestinal passage and their interaction with transglutaminase and/or the immune system. A deeper understanding of the microbiota could also provide different therapeutic strategies, aiming to degrade gliadin or to reduce the inflammatory milieu.

This Special Issue could thus represent a collection of the current knowledge about celiac disease, ranging from genetics to new therapies; for this reason, I am glad to invite all our colleagues working in this field to contribute to this new Special Issue with reviews or original data.

Dr. Donatella Barisani
Guest Editor

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• celiac disease
• gliadin
• gluten
• innate immunity
• adaptive immunity
• gene expression
• transglutaminase
• epigenetics
• miRNA
• incRNA