Research from Uppsala University reveals that interleukin-35 reverses of cures type 1 diabetes.

protein2 is one of the hardest to manage and almost impossible to reverse, usually requiring a life-long dependence of daily injections of insulin. A new study from Uppsala University has indicated a new treatment for involving interleukin-35 (a produced by immune cells).

The reverses of cures by maintaining a normal level and impacts on the immune system as is considered an .

The scientists used a mouse model to investigate so-called immune regulatory ’ actions in T1D mouse models. The study shows that the immune regulatory alter their function by producing pro-inflammatory destructive proteins instead of protective anti-inflammatory proteins such as interleukin-35 (IL-35) under T1D conditions.

Mice were injected with a chemical to induce . These mice developed signs of TID and levels similar to humans suffering from . IL-35 injections given after disease induction prevented the mice from developing T1D. Mice who were diabetic for two consecutive days were normalized after IL-35 injections and their diabetes was reversed.

“This suggests that the good guys have gone bad in early development of and therefore our immune cells destroy the ,” said Dr. Kailash Singh, a PhD student in professor Stellan Sandler’s group at the Department of Medical Cell Biology at Uppsala University.

“To the best of our knowledge, we are the first to show that IL-35 can reverse established in two different mouse models and that the concentration of the particular cytokine is lower in patients than in healthy individuals. Also, we are providing an insight into a novel mechanism: how immune regulatory change their fate under autoimmune conditions,” said Dr. Kailash Singh.


Kailash Singh, Erik Kadesjö, Julia Lindroos, Marcus Hjort, Marcus Lundberg, Daniel Espes, Per-Ola Carlsson, Stellan Sandler, Lina Thorvaldson. Interleukin-35 administration counteracts established murine – possible involvement of regulatory . Scientific Reports, 2015; 5: 12633 DOI: 10.1038/srep12633

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