City of Hope researchers have uncovered a potential new path to treating type 1 diabetes. The finding also may point to new treatments for other autoimmune diseases.
 Han Qin, left, and Chih-Pin Liu study a protein that might lead to a treatment for autoimmune diseases. (Photo by Darrin S. Joy) |
Scientists led by Chih-Pin Liu, Ph.D., professor in the departments of Diabetes and Metabolic Diseases Research and Immunology, found high levels of a specific protein in the cells that control the body’s response to disease. The protein could present a new target for researchers developing drugs to combat type 1 diabetes and other autoimmune diseases.
They reported their findings in the Feb. 1 issue of the Proceedings of the National Academy of Sciences.
Like a vast army of soldiers standing guard, cells of the immune system remain ready to destroy diseased cells and defend the body from bacteria and other invaders. These soldier cells normally leave healthy cells alone, however, because the immune cells are tightly controlled by special agents called regulatory T cells, or Treg cells.
In autoimmune disease, Treg cells lose their authority, so the immune cells begin attacking healthy tissues. For those with the autoimmune disease known as type 1 diabetes, this attack targets cells that produce insulin, which helps the body turn sugar from food into energy. The resulting buildup of sugar in the blood can lead to severe and life-threatening complications such as blindness, nerve damage and kidney failure.
In the recent study, the scientists found that a protein called KIR3DL1 appears to be to blame for the faulty regulation. When Treg cells produce too much of the protein, they lose control of the immune cells.
“When we analyzed Treg cells in mice prone to develop type 1 diabetes, we found their Treg cells had elevated levels of the protein,” Liu said. After the researchers knocked down the Treg cells’ ability to produce KIR3DLI, the Treg cells regained control of the immune cells and kept them from attacking insulin-producing cells.
“Our results suggest that molecules that can hinder the protein could help return the immune system to normal and alleviate diabetes or other autoimmune diseases,” said Liu. More research is needed, but identifying KIR3DLI has now allowed researchers to begin searching for drugs that can inhibit it, he added.
Other City of Hope researchers on the study include Hanjun Qin, Ph.D., Zunde Wang, Ph.D., Weiting Du, Ph.D., Wen-Hui Lee, Xiwei Wu, M.D., Ph.D., and Arthur Riggs, Ph.D. The study was supported by funds from the Juvenile Diabetes Research Foundation, the American Heart Association, the American Diabetes Association, the National Institutes of Health and the H.L. Snyder Medical Foundation.
