An Indian origin scientist has revealed an anti-inflammatory small protein which might cure type 2 diabetes by maintaining a normal blood glucose level and the immune tolerance.
New research from Uppsala University reveals that the administration of interleukin-35, a protein made by immune cells, to mice with type 1 diabetes, reverses the disease.
Dr. Kailash Singh, a PhD student at Uppsala University from professor Stellan Sandler’s research group , studied so-called immune regulatory T cells’ actions in type one diabetes mouse models.
The study shows that the immune regulatory T cells alter their function by producing pro-inflammatory destructive proteins instead of protective anti-inflammatory proteins such as interleukin-35 under type 1 diabetes conditions.
Dr Singh said that this suggests that the good guys have gone bad in early development of type 1 diabetes and therefore our immune cells destroy the beta cell.
Furthermore, the concentration of interleukin-35 was lower in type 1 diabetes patients compared to healthy individuals. These findings may suggest that interleukin-35 could play a crucial role in human type 1 condition.
Additionally, the researchers also found a novel mechanism that explains how the immune regulatory T cells are changing their destiny under a type one diabetes condition.
The team tested whether or not interleukin-35 could also suppress development of type 1 diabetes and reverse established type 1 diabetes.
To induce type 1 diabetes in mice, the team injected a chemical compound called streptozotocin. These mice developed signs of type 1 diabetes and increasing blood glucose levels similar as in human type 1 diabetes.
Interleukin-35 injections given after disease induction prevented from development of type 1 diabetes. Noticeably, Interleukin-35 injections to mice normalised blood glucose concentrations.
The research team also successfully investigated interleukin-35 in another model of type 1 diabetes called non-obese diabetic mouse (NOD). The interruption of interleukin-35 treatment did not result in return of diabetes in any of the mouse models.
Dr Singh said that they provided an insight into a novel mechanism: how immune regulatory T cells change their fate under autoimmune conditions.
The study is published in the journal Scientific Reports.