Seventy percent of mice that got transplants two days after they became hyperglycemic did not need immunosuppression, the Canadian researchers found; after nine days, the acceptance rate was reduced to about 10 percent. "The question is why?" Dr. Pacholczyk said.
Typically the path isn't easy for transplanted cells. Many die from the stress of transplantation or immune system attack either because they are rejected as invaders or because the same autoreactive mechanism that led to destruction of the patient's own cells is resurrected. "Cells that survive are the ones being counted on. Over time, they should increase in mass to a level that should produce sufficient amounts of insulin," the researcher said.
Type 1 diabetes results from the wrong mix of genes and environmental triggers. For example, early exposure of a genetically predisposed child to cow's milk and a viral infection could trigger an immune response to bovine insulin which, in turn, leads to islet cell destruction.
The researcher's animal model reflects the human condition fairly well; it's inbred to have diabetes but Dr. Pacholczyk developed a system to chemically induce the disease when he wants so he'll know exactly when islet cells are destroyed by the immune system. He'll document hyperglycemia's impact on all immune cells with the long term goals of identifying the magic that enables acceptance of islet cells and finding a safer, more direct way to replicate it.
In 2007, he and colleague Dr. Leszek Ignatowicz caused a stir in the scientific community when th
|Contact: Toni Baker|
Medical College of Georgia