People who receive organ transplants need to take immunosuppressive medications, to keep their bodies from rejecting the new organ. This therapy is complex and expensive. Past immunosuppressants, while successful for kidneys, even hearts, have been demonstrated toxic for islet cell transplants. The search is on for better ways to control immunosuppression.
Researchers from the St. Vincent's Institute, of Melbourne, Australia, are following a new line of inquiry. Like an infection, an immunosuppressive/autoimmune attack upon an organ produces inflammation -- and it is that inflammation that damages or destroys the organ.
A molecule named SOCS1 appears to do two jobs: As part of an islet-cell transplantation, it reduces (and may eliminate) the need for traditional immunosuppressants, and, given to mice expected (and bred) to develop type 1 diabetes, it shielded their beta cells from the inflammation that would have destroyed them, producing diabetes. In so many words, SOCS1, given at the right time, prevented the onset of type 1 diabetes.
With luck, these findings will translate into better human immunosuppression, and, perhaps (as current findings are based on animal research) a way of intervening against the autoimmune assault that causes type 1 diabetes, and several other diseases, perhaps Systemic Lupus or Multiple Sclerosis.
It'll be a while. If laboratory testing is successful, look for SOCS1 to be used with islet cell transplants within the next five years.