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The endomysium contains a form of transglutaminase called "tissue transglutaminase" or "tTG" for short, and antibodies that bind to this form of transglutaminase are called endomysial autoantibodies (EmA). [6] The antiendomysial antibody test is a histological assay for patient serum binding to esophageal tissue from primate.
Anti-transglutaminase antibodies result in a form of gluten sensitivity in which a cellular response to Triticeae glutens that are crosslinked to tTG are able to stimulate transglutaminase specific B-cell responses that eventually result in the production of anti-transglutaminase antibodies IgA and IgG.
Antibody recognition of gluten is complex. Direct binding to gluten such as anti-gliadin antibodies has an ambiguous pathogenesis in coeliac disease. The crosslinking of gliadin with tissue transglutaminase leads to the production of anti-transglutaminase antibodies, but this is mediated through T-cell recognition of gliadin.
Persons suspected of having celiac disease may undergo serological testing for IgA anti-tissue transglutaminase antibodies (abbreviated anti-tTG antibodies or anti-TG2 antibodies) and anti-endomysial antibodies (abbreviated EMA) provided the IgA-level is high, and if IgA is low, testing for certain IgG antibodies; in case of positive ...
The IgG antibody is similar to AGA IgA, but is found at higher levels in patients with the IgA-less phenotype. It is also associated with coeliac disease and non-celiac gluten sensitivity. [5] [6] [7] Anti-gliadin antibodies are frequently found with anti-transglutaminase antibodies.
Some instance of arthritis with small bowel villous atrophy have been found to resolve on gluten free diet, [93] and anti-connective tissue antibodies have been found in increased levels in coeliac disease. [94] Anti-rheumatoid factor antibodies are also increased. [95]
[7] [22] NCGS and celiac disease cannot be separated in diagnosis because many gastrointestinal and non-gastrointestinal symptoms are similar in both diseases, [22] [29] [30] and there are people with celiac disease having negative serology (absence of specific celiac disease antibodies in serum) or without villus atrophy.
Additionally, the concomitant diagnosis of Celiac disease can be made without the need for a small-intenstinal biopsy if an individual has biopsy-confirmed dermatitis herpetiformis as well as supporting serologic studies (elevated levels of IgA tissue transglutaminase antibodies, IgA epidermal transglutaminase antibodies, or IgA endomysial ...