Multiple factors probably play a role, but evidence indicates that one big factor is the intestinal microbiota.
However, in people with celiac disease, certain cells (known as antigen-presenting cells) get a hold of these large, undigested fragments of protein and present them to T-cells, triggering an immune response.
( 13 this fits with previous work done by researchers such as Alessio Fasano, who have hypothesized that a person cannot develop an autoimmune condition such as CD if they dont have leaky gut.
A recent study (hat tip to Questioning Answers for the find) found that an overabundance of the yeast Candida albicans could contribute to the development of CD, and unfortunately, antibiotic use is a big risk factor for developing a candida infection.
And a major contributor to disordered intestinal microbiota is antibiotic overuse.
Antibiotics can cause intestinal dysbiosis and infection.Remember how tissue transglutaminase (TG2) readily binds gliadin?This attack of self is what earns CD the classification of autoimmune.( 11, 12 ) This indicates that tissue damage or inflammation in the intestine (and subsequent TG2 up-regulation) might actually be necessary for the development.Celiac disease involves an immune reaction to both gliadin and tissue transglutaminase.
Bacterial components such as lipopolysaccharides can induce inflammation and increase intestinal permeability, which would allow gluten into the sub-epithelial region of the intestine where it could be modified by TG2 and trigger.
In other words, genetics appear to be necessary but not sufficient for someone to develop.
Gliadins and glutenins are the two main components of gluten, with gliadins being the primary trigger for celiac disease.