Interleukin-35 is a cytokine produced by regulatory T cells and plays an important role in immune suppression. The immune agent has previously been studied for its potential in treating Type-1 diabetes. In animal models, this cytokine is found to stop the immune attack against insulin-producing beta cells.
A new study by researchers at the Uppsala University not only proves that it could have a similar effect in humans, but it shows it could be a natural process capable of being manipulated to reduce or stop the progression of the disease.
The result of this study was counterintuitive, given it showed that out of a total of 113 diabetes patients who had been living with the disorder for more than 10 years now that were tested, about 41% still presented residual insulin production.
The researchers confounded by the result then set out to study what made these patients different since Type-1 diabetes is expected to lead to a complete exhaustion of insulin. They analyzed the levels of circulating cytokines and found that the patients that could still produce some insulin had much higher blood levels of IL-35, as well as more IL-35-producing B- and T-cells.
A previous study by the same group had
earlier elucidated that the levels of IL-35 in type 1 diabetics, both newly diagnosed and long-term sufferers, exhibited lower levels of the cytokine as compared to healthy people.In light of this new evidence, the group is now looking forward to a new study design involving tests to determine whether IL-35 could be responsible for the regeneration of insulin-producing cells in diabetic patients.
