Protein fragments may trigger type 1 diabetes in mice
A study at National Jewish Health and the University of Colorado Anschutz Medical Campus has revealed a protein fragment that may be responsible for triggering type 1 diabetes in mice.
Although T cells are protective components of the immune system, some of them have the potential to cause autoimmune disease. During the development of these cells in the thymus, they are exposed to protein fragments that help pinpoint and destroy the ones that may cause damage. However, the process is not foolproof and some are able to escape.
MHCII, the molecule that presents fragments of protein to the immune system, has been associated with type 1 diabetes in mice. This molecule can present a fragment of insulin in four different combinations of amino acids, called registers, to the T cells.
Researchers discovered that the register that bound most weakly to MHCII was the one that stimulated diabetes-associated T cells.
John Kappler, an immunology professor at National Jewish Health, said that this is not the first time that a specific peptide and its binding register have been associated with autoimmune disease. All three have been peptides that are weakly bound to the MHCII molecule.
The research team hopes that this preliminary finding will help in developing treatments in the future.