In a new study published in Science, researchers identify a mechanism in mice by which the nervous and immune systems interact to regulate blood glucose levels by controlling pancreatic glucagon secretion.

First, they observed that mice with no adaptive lymphocytes and innate lymphoid cells (ILCs) (Rag2−/−Il2rg−/−) had reduced blood glucose and glucagon levels during fasting. But this effect was not observed in mice that only lacked adaptive lymphocytes, which implicated ILCs in glucose regulation. Specifically, transplanting group 2 ILCs (ILC2s) into mice lacking lymphocytes increased fasting blood glucose levels and secretion of pancreatic glucagon, a hormone that regulates blood glucose levels. In vitro observations suggested that cytokines produced by pancreas-resident ILC2s increased secretion of glucagon by α-cells in the islets of Langerhans.