Your support of JDRF’s plan to turn Type One into Type None has led to real progress. Because of you, research advances like these are possible. Thank you for your commitment to JDRF.
IMMUNE CELLS PROMOTE BETA CELL GROWTH
Developing therapies to regenerate beta cells lost in T1D is a high priority for JDRF, as they could help people with the disease achieve insulin independence. Now, JDRF-funded researchers at Joslin Diabetes Center are closer to that goal.
Data from Joslin’s 50-Year Medalist Study has shown that some people retain some beta cells decades after their diagnosis. Researchers have long suspected that immune cells may play a role in beta cell preservation, but exactly how remained a mystery.
In a first-of-its-kind study, Joslin scientists injected nonobese diabetic (NOD) mice with immune cells—subtypes of T cells and B cells—from the pancreatic islets of donor NOD mice. They observed that beta cell growth occurred after the host islets were infiltrated by the immune cells, and that it is specifically the T cells, not the B cells, that are associated with that growth. Further, they found that the immune cells secrete inflammatory cytokines and chemokines—signaling proteins—that work together to enhance beta cell growth.
These results are encouraging. The investigators will next move on to human beta cells and aim to determine whether those signaling proteins can be harnessed to elicit beta cell proliferation.
PREVENTING T1D WITH ANTICANCER DRUGS
Repurposing drugs indicated for other diseases is one of JDRF’s approaches to accelerating the delivery of new therapies to people with T1D. A recent JDRF-funded study in mice determined that low doses of a cancer drug protect against the development of T1D—bringing us one step closer to a potential preventive treatment.
Researchers at three Danish universities investigated lysine deacetylase inhibitors—a well-tolerated class of lymphoma drugs—because of their ability to block the molecules that send harmful inflammation signals to pancreatic beta cells. Extremely low doses—doses 100 times lower than those used in cancer treatment—protected the mice’s beta cells from the destructive effects of inflammation and ultimately prevented the development of T1D in the mice. In additional tests, this time on insulin-producing human donor tissues already exposed to the inflammation, the drug delayed the destruction of beta cells.
The next step for the research team is to test the drug on those at risk of developing T1D. JDRF will work closely with the investigators as they move forward with this critical step in the translational research process, which is a key part of JDRF’s plan to create a world without T1D.