A drug currently used to treat psoriasis is effective in treating the early stages of type 1 diabetes in children and adolescents, a new clinical trial led by Cardiff University in the UK has shown. Researchers have found that ustekinumab, an immunotherapy that has been used to treat psoriasis since 2009, is effective in preserving the body’s ability to produce insulin in type 1 diabetes, bringing the goal of managing the disease without the need for insulin closer to being achieved.
The study, conducted by Cardiff University, King’s College London, Swansea University and the University of Calgary, has revealed new insights into the specific immune cells (Th17 cells) that cause type 1 diabetes and established the role of immunotherapies in halting the destruction of insulin-producing cells. The trial tested the psoriasis treatment in 72 adolescents aged 12 to 18 years with recent-onset type 1 diabetes. The study’s findings have been published in Nature Medicine.
“Type 1 diabetes occurs when the body’s immune system attacks and destroys the cells that produce insulin. This leaves the person dependent on insulin injections. Researchers are now developing ways to slow down or stop the immune system’s attack. If these treatments can be started early, before all insulin-producing cells are lost, this could prevent or reduce the need for insulin,” explained Dr Danijela Tatovic.
Researchers hope that immunotherapy will help patients in the future by targeting the body’s immune system to slow the destruction of cells that produce insulin. This treats the underlying immune process rather than correcting insulin levels.
Controlling childhood diabetes with a psoriasis drug
Ustekinumab is an injectable treatment that patients can administer themselves at home and is used effectively in the treatment of a large number of patients with autoimmune diseases, including severe psoriasis, psoriatic arthritis, severe Crohn’s disease and severe ulcerative colitis.
This study showed that ustekinumab can also preserve vital insulin-producing cells. The researchers also identified the specific immune cells that cause this destruction, allowing for precise, targeted therapies to maximize benefits and minimize side effects.
“We found that ustekinumab reduces the level of a small group of immune cells in the blood called Th17.1 cells. These cells make up just 1 in 1,000 of the immune cells in the blood, but they appear to play an important role in destroying insulin-producing cells,” said Professor Tim Tree, from King’s College London. “This explains why ustekinumab has so few side effects. It targets the problem cells and leaves 99% of the immune system intact – a great example of precision medicine.”
Ustekinumab can also preserve vital insulin-producing cells, allowing for precise, targeted therapies to maximize benefits and minimize side effects.
Ustekinumab was shown to decrease the destructive impact of Th17 immune cells on insulin-producing cells. After 12 months of using ustekinumab, researchers found that levels of C-peptide, a sign that the body is producing insulin, were 49% higher. This clinical trial also provides the first clinical trial-based evidence of its role in Th17 cells in type 1 diabetes.
While the trial demonstrates the benefit of using ustekinumab to treat type 1 diabetes, further clinical trials are needed to confirm this finding and determine which patients would benefit most from the treatment. “It is now possible, with a simple finger-prick antibody test, to detect children who will develop type 1 diabetes years before they need insulin. Combining screening in this way with early treatment with ustekinumab seems a very promising approach to preventing the need for insulin. Further trials will be needed to confirm this,” concludes Peter Taylor, Professor at Cardiff University’s Systems Immunity Research Institute.
