The findings, reported in the June 7 issue of the Journal of Experimental Medicine, prove an important biological principle that could lead to prevention of Type 1 diabetes in humans: autoimmunity can be reversed if the immune system's mechanisms for tolerance -- recognition and acceptance of the body's own cells -- can be repaired.
Using immune system cells called dendritic cells to stimulate increased numbers of suppressor T cells, which turn off the body's immune response, the research team rescued mice from the destruction of their pancreatic islet cells that causes Type 1 diabetes. The research was led by Kristin Tarbell, Ph.D., a postdoctoral associate in Rockefeller's Laboratory of Cellular Physiology and Immunology, headed by professor and senior physician Ralph Steinman, M.D.
"You have to stop the immune system from attacking those pancreatic islet cells," says Tarbell. Otherwise, even with the possibility of islet cell transplants, the same process that destroyed the first set will destroy the second, Tarbell explains.
"Instead of silencing the attackers directly, we learned how to generate another type of cell, called a regulatory or suppressor cell, which essentially turns off the attackers. Basically, it's a numbers game, and the problem in the onset of this disease is that there are not enough of the regulatory cells that suppress the immune response against the body's insuling-producing pancreatic islet cells," says Tarbell. Putting the right number (in the case of mice, 5000 to 50,000) of regulatory T cells where they are needed arrests the onset of Type 1 diabetes in the animals.
This research used a special source of T cells from mice genetically altered to have a majority of cells directed to the islets. Now Tarbell will exten
Contact: Lynn Love