Anti-inflammatory protein may help treat type 1 diabetes, claims Indian scientist

2 years ago | 31-07-2015 | ANI

Washington DC, July 31 : An Indian origin scientists 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.