Scientists at Yale University recently found a mechanism of action by which Teplizumab, an anti-CD3 antibody may be working as an immune therapy for Type 1 diabetes.
Teplizumab, the drug used in the study, is thought to work by shutting off a part of the immune system most responsible for attacking these insulin-producing cells and generating long-term immunoregulation to control this misguided autoimmune response. While previous trials tested whether Teplizumab might preserve insulin production in people recently diagnosed with T1D, researchers are now also studying whether the drug might preemptively prevent or delay the development of T1D in at-risk individuals. One such study is being conducted by the National Institutes of Health’s Type 1 Diabetes TrialNet.
Currently, once T1D starts to develop, there’s no intervention developed to stop it. The immune system slowly and inevitably kills the pancreatic beta cells that produce insulin, a hormone that enables people to get energy from food. As a result, people with T1D have to test their blood sugar and give themselves insulin (with injections or an insulin pump) multiple times every day in order to stay alive. What’s more, reversing T1D remains an elusive and complicated challenge, requiring restoration of the insulin-producing cells that were destroyed, as well as solutions to turn off the misguided immune system attack on insulin-producing cells.
The latest findings about Teplizumab are reported in the current issue of the journal Science Translational Medicine.
News Release courtesy of JDRF.org.