Celiac: A prototype for chronic, inflammatory, and autoimmune diseases

Today, increasing chronic inflammatory diseases such as epidemics have become a serious socioeconomic problem for developed western societies and developing countries. In this respect, clarification of the pathogenesis mechanism of autoimmunity and inflammation will be a guide for the prevention and treatment of chronic diseases. Despite intensive research, the pathogenesis mechanism of autoimmune diseases has not been resolved. Since autoimmune and inflammatory mechanisms coexist in pathogenetic processes, these two components are often referred to together. Since inflammation is the main pathogenetic component of chronic diseases, autoimmune diseases are also the most important component of the chronic disease burden. We think that the pathogenetic mechanism seen in celiac disease may be a prototype for other autoimmune and inflammatory diseases, since the etiological factor in celiac disease is clear and the autoimmune and inflammation component is clearly known here. In this context, celiac pathogenesis may also be a guide for understanding autoimmune and inflammatory pathogenesis. Although there are some issues that have not been clarified for autoimmune mechanisms in the pathogenesis of celiac, Tool Like and GPCR receptor pathways, which are constantly active with chronic stimulation of the immune system by gluten and gliadin, seem to be responsible for the continuity of inflammation. In the mechanism operating through these two pathways, retinoic acids are depleted. Indeed, retinol deficiency in celiac patients has been reported in previous studies. However, no association has been made regarding the role of retinol and retinoic acids in the pathogenesis of celiac. It has been previously reported that retinol depletion and related retinoid signaling defect and associated immune dysregulation are responsible for inflammation and autoimmune pathogenesis in autoimmune diseases. In this study, chronic irritation of the immune system through gluten and gliadin in celiac, and the resulting impaired retinoid signaling mechanism and immune system dysregulation will be discussed in the light of current literature. We argue that the retinoid signaling mechanism is a common pathogenetic pathway for celiac as well as many inflammatory and autoimmune diseases.