A study at Uppsala University has recently shown the potential of an anti-inflammatory cytokine for Type 1 diabetics.
Type 1 diabetes (T1D) is an autoimmune disease in which the host's immune cells attack beta-cells in their pancreas where insulin is produced, initiated due to an infection or a plethora of factors. Insulin is central to glucose control in the blood and preventing levels from becoming too high or too low. Sweden alone reports 2 new cases of T1D every day, in which patients are confined to lifelong treatment of daily insulin which can be costly and limiting for the patient.
Stellan Sandler's research group at the Department of Medical Cell Biology at Uppsala University have found that regulatory T cells--important in the immune attack against the beta cells--alter their behavior early on in the progression of the disease and transition from anti-inflammatory to pro-inflammatory. Anti-inflammatory proteins such as interleukin 35 (IL-35) are known to be protective, whereas pro-inflammatory proteins are destructive in nature.
Their work was published in the open access journal Scientific Reports (Nature Publishing Group). Kailash Singh, who is one of the members of the team, 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."
Their approach was twofold. First they found that IL-35 was lower in patients with T1D compared to healthy controls and then consequently using this clinically relevant target injected IL-35 into chemically induced T1D mice, which caused their blood glucose to return to normal levels.
They followed up in another mouse model of T1D that are genetically predisposed to T1D and found the same was true--diabetes did not return in these mice after IL-35 treatment.
"To the best of our knowledge, we are the first to show that IL-35 can reverse the established Type 1 diabetes in two different mouse models that the concentration of the particular cytokine is lower in Type 1 diabetes patients that in healthy individuals. Also, we are providing an insight into a novel mechanism: how immune regulatory T cells change their fate under autoimmune conditions," says Singh.