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Concept
Anti-transglutaminase antibodies
Summary
Anti-transglutaminase antibodies (ATA) are autoantibodies against the transglutaminase protein. Antibodies serve an important role in the immune system by detecting cells and substances that the rest of the immune system then eliminates. These cells and substances can be foreign (for example, viruses) and also can be produced by the body (for example, cancer cells). Antibodies against the body's own products are called autoantibodies. Autoantibodies can sometimes errantly be directed against healthy portions of the organism, causing autoimmune diseases.
ATA can be classified according to 2 different schemes: transglutaminase isoform and immunoglobulin reactivity subclass (IgA, IgG) toward transglutaminases.
Antibodies to tissue transglutaminase (abbreviated as anti-tTG or anti-TG2) are found in patients with several conditions, including celiac disease, juvenile diabetes, inflammatory bowel disease, and various forms of arthritis.
In celiac disease, ATA are involved in the destruction of the villous extracellular matrix and target the destruction of intestinal villous epithelial cells
by killer cells. Deposits of anti-tTG in the intestinal epithelium predict celiac disease.
The endomysium is a layer of connective tissue that ensheaths a muscle fiber. 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).
The antiendomysial antibody test is a histological assay for patient serum binding to esophageal tissue from primate. EmA are present in celiac disease. They do not cause any direct symptoms to muscles, but detection of EmA is useful in the diagnosis of the disease.
Antibodies to epidermal transglutaminase (eTG, also keratinocyte transglutaminase) are the autoantibodies believed to cause dermatitis herpetiformis.
ATA IgA are more frequently found in Celiac Disease (CD); however, ATA IgG are found in CD and at higher levels when affected individual had the IgA-less phenotype.
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