Vaccine to Suppress Type 1 Onset in At-Risk Children Could Be Based on Enzyme


By: dhtest

Georgia researchers believe that a powerful enzyme that inhibits or modifies immune system response could be the basis for a vaccine administered to children at high risk for developing type 1 diabetes.

Unlike most vaccines, which work by “teaching” the immune system to attack something, this one would instruct it to avoid attacking pancreatic beta cells-the haywire autoimmune response responsible for the onset of type 1.  

The enzyme, called indoleomine 2,3-dioxegenase (IDO), is an immune system inhibitor that fetuses use to fend off or prevent an immune response directed against them by their mothers’ bodies. 

In their experiments with IDO, scientists at the Medical College of Georgia Immunotherapy Center in Augusta bundled the enzyme with dendritic cells, which are the cells that “tell” the body’s powerful T cells to launch an attack.  Apparently the dendritic cells’ association with IDO was enough to keep the body’s powerful immune system warriors pacified.

Children at risk of developing type 1 do not have any or enough IDO associated with their dendritic cells, which leads them to invite T cell attacks on pancreatic beta cells. A vaccine that could increase dendritic cells’ association with IDO would prevent, perhaps permanently, the T cell attack that eventually destroys the insulin-producing capability in patients’ pancreases and signals the onset of type 1.



Diabetes Health Medical Disclaimer
The information on this site is not intended or implied to be a substitute for professional medical advice, diagnosis or treatment. All content, including text, graphics, images, and information, contained on or available through this website is for general information purposes only. Opinions expressed here are the opinions of writers, contributors, and commentators, and are not necessarily those of Diabetes Health. Never disregard professional medical advice or delay seeking medical treatment because of something you have read on or accessed through this website.