First in a two-part series on transplant tolerance. Read part two.
Although organ transplant recipients take drugs to suppress the inflammatory immune response, almost all eventually lose their transplant. A new approach, perhaps added to standard immunosuppressant treatment, could greatly enhance people’s long-term transplant tolerance, report researchers at Boston Children’s Hospital.
The approach, which has only been tested in mice as of yet, works by maintaining a population of T cells that naturally temper immune responses. It does so by turning on a gene called DEPTOR, which itself acts as a genetic regulator. In a study published July 3 in the American Journal of Transplantation, boosting DEPTOR in T cells enabled heart transplants to survive in mice much longer than usual. …
Most adult transplant centers require patients to walk a set distance in under six minutes to remain a good candidate for lung transplant. The thought is that if patients cannot meet this minimal threshold, then their chances of being able to rehabilitate after transplant are diminished. In pediatrics, this is also important. But Dawn Freiberger, RN, MSN, Boston Children’s Hospital’s Lung Transplant coordinator, says there are other factors that have to be considered.
“The walk test is just one piece of the pie,” says Freiberger.
Chronic, unresolved inflammation can be quite harmful, right down to the cellular level. At the macro level, it has links to cancer, diabetes, heart disease and other degenerative conditions.
This is why the body keeps a tight rein on the inflammatory response and maintains a host of factors that resolve inflammation once the need for it (for instance, to clear an infection or heal an injury) has passed.
We know pretty well which factors work between cells to turn on and turn off inflammation. That knowledge has led to the development of drugs like ibuprofen, acetaminophen and naproxen, all of which temper pro-inflammatory factors.
However, when you look at the signals and signaling pathways within cells, things get more complex, especially when it comes to factors that turn off inflammation. We haven’t completely grasped the full complement of proteins that transmit these internal anti-inflammatory signals. If we did, we could potentially add new drugs to our pharmacopeia to regulate or resolve inflammation or maintain cells in a non-inflamed state, and perhaps help prevent rejection of transplanted organs and tissues.
David Briscoe, MD, and his team at Boston Children’s Hospital’s Transplant Research Program, has taken the field one step closer to grasping those internal pathways by studying a cellular protein called DEPTOR. …