Project
Background
Motivation
Celiac disease is a serious autoimmune disorder that is mainly caused by gluten, which is composed of gliadorphins. Among gliadorphin, amino acid called proline is abundant. This proline causes inflammation in intestinal immunocyte, triggering it to attack absorptive cells and damage small intestine.
This phenomenon causes celiac disease; in order to prevent this, enzyme called DPP4 is used. DPP4(Dipeptidyl peptidase-4) breaks proline down into dipeptide form in n-terminal as the picture explains.
However, the last tripeptide(gln-pro-phe) does not fully break down and eventually inhibits DPP4, slowing down its process. Therefore, additional input of DPP4 is important in digestion to catch up with the inhibition.
As the graph explains, the increasing incidence and altered presentation in a population-based study of pediatric celiac disease in North America was discovered. However, only temporary solutions exist: taking pills regularly or simply regulating the intake of gluten. From 2004 to 2005, sales of gluten-free foods increased by 77.8 million dollars (a growth of 14.6%). We discovered that more people are relying on temporary solutions and fundamental solution is needed, so that they can eat the gluten freely.