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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.
Even if a person doesnt develop an overt, clinically-diagnosable infection such.Now Id like to hear from you.In healthy individuals, TG2 plays a role in tissue repair, as well as in other processes such as regulation of cell death; its not an enzyme thats supposed to interact with gluten.By signing up, you agree to our privacy policy.Intestinal dysbiosis and infection can contribute to leaky gut.( 7, 8 an enzyme called tissue transglutaminase (TG2) is also important in the development.But one big risk factor for developing leaky gut is intestinal dysbiosis or infection.But to understand how antibiotic-induced gut dysbiosis could trigger celiac disease in genetically-susceptible individuals, it helps to first understand some of the basic mechanisms behind celiac disease.( 9 ) On the other hand, TG2 readily binds lucky chances casino colma ca gliadin, and actually modifies it to make the gliadin much more attractive to antigen-presenting cells.



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.


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