NewHopeBlog has published more information related to a report about the mechanisms leading to Type I diabetes:
The results of long-term studies indicate that insulin is the trigger that unleashes autoimmune lymphocytes to attack beta islet cells in the pancreas that produce insulin. Could a therapeutic approach to preventing the lymphocytes from attacking the beta islet cells [perhaps by a mechanism of CD8+(T-suppressor cell) activation] involve controlling NKT-cell activity – a hot target of current research in autoimmune diseases? Could ineffective NKT cell-mediated immunoregulation in autoimmune-prone individuals such as with nonobese diabetic (NOD) mice be related to defective signals that regulate CD1d(the NKT cell restriction molecule) expression at time and site of autoimmunity? Let’s look at the news report of the research indicating that insulin is the trigger, and you can see that these questions just might fit the article like OJ’s glove:
AFP via Yahoo
Researchers believe they have made an important breakthrough in understanding the severest form of diabetes, confirming that the disease begins when the body’s immune system reacts to the hormone insulin.
Type 1 diabetes usually occurs in childhood, when immune cells called lymphocytes start to attack beta islet cells that make insulin in the pancreas. A vicious circle then starts up. The remnants of the beta cells are transported to a draining lymph node in the pancreas, where they attract the attention of immune-system scouts, which in turn prime more lymphocytes to destroy more beta cells.
After 80-90 percent of the beta cells have been wiped out, the first clinical symptoms of diabetes show up.
The pioneering work by University of Colorado scientist George Eisenbarth and colleagues indicates that insulin is the trigger which unleashes autoimmune lymphocytes. The discovery throws up exciting avenues for potential treatment, perhaps by wiping out the aggressive cells or preventing them from going on the offensive in the first place, he said.