Celiac disease is the over reaction of the immune system to gluten proteins. More specifically, the enzyme transglutaminase 2 or TG2 in the small intestine modifies the gluten molecule thus inducing the immune response in the small intestine.

Non-celiac or “normal” people have lots of TG2 floating around in their small intestine. This TG2 can be active or inactive. If the TG2 is inactive nothing happens or the small intestine is in the normal state. If there is a forming or breaking of the bond between two amino acids in the TG2 enzyme, gluten induces the overactive immune response. The bond that breaks or forms is the disulfide bond within the enzyme. This breaking of the disulfide bond is what “turns” on the immune response.

Scientists have figured out what enzyme Erp57 breaks this bond. Now the question is, can they control it? Are there unintended consequences to keeping this bond in tact? They think not, because everyone has this TG2 enzyme – its just in those with Celiac disease its broken.

This might be the start of a whole new class of drugs or it might be just new information. We don’t know and nor do they. But I’m glad to see that they are still learning new things about celiac disease and how it works. The more they know, the closer we are to a cure!

Summary of article and hardcore science article.

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