Increasing a specific protein in areas of the pancreas that produce insulin, blocks the immune attack that causes type 1 diabetes, indicates new research.
The discovery could lead to a drug that prevents the progression of type 1 diabetes in people newly diagnosed who are in the "honeymoon" phase of the disease, when the immune system has not yet destroyed all of the insulin-producing beta cells in the pancreas.
The finding could also lead to new drugs for overcoming organ rejection in transplant patients and for improving the survival of transplanted islets - the clusters of cells in the pancreas that contain beta cells.
Normally, as the immune system successfully defeats an infection, a special type of white blood cell called T-regulatory cells produce chemical signals that turn off the immune response.
The researchers took advantage of this phenomenon as they sought to protect the beta cells from immune attack.
They used a modified virus to insert the gene for a protein called CCL22 into the beta cells of a strain of mice known to develop diabetes. The gene caused the beta cells to produce the CCL22 protein. This attracted T-regulatory cells, which blocked the attacking immune cells and prevented most of the mice from developing type 1 diabetes.
"It's a novel way to turn down the immune system specifically in the region of the beta cells inside the pancreas, and that may be a big advantage over general immune suppression, which can have significant side effects," said Dr. Bruce Verchere, one of the study's principal investigators. He is head of the diabetes research program at the Child and Family Research Institute (CFRI) at BC Children's Hospital, Irving K Barber Chair in Diabetes Research, and professor, Department of Pathology and Laboratory Medicine and Department of Surgery at the University of British Columbia (UBC).
The study will be published in the Journal of Clinical Investigation.