The role of insulin as a boost to the immune system to improve its ability to fight infection has been detailed for the first time by Toronto General Hospital Research Institute (TGHRI) scientists.
TGHRI scientists have identified a specific insulin signaling pathway that, when activated, revs up the response of T cells in the immune system to divide rapidly and secrete cytokines, chemical messenger proteins that activate the rest of the immune system.
A fast and effective immune response protects us against disease and life-threatening infections by destroying infected cells or microbes, while a wrong or inefficient one can cause immune system disorders or diseases to develop.
The research findings are published today in a paper called, "Insulin receptor mediated stimulation boosts T cell immunity during inflammation and infection," in
Cell Metabolism, by first author Dr. Sue Tsai, postdoctoral fellow, and senior authors, Dr. Daniel Winer, Anatomical Pathologist, UHN, TGHRI, and Dr. Shawn Winer, Anatomical Pathologist, St. Michael's Hospital.
"We have identified one of metabolism's most popular hormones, specifically the insulin signaling pathway, as a novel 'co-stimulatory' driver of immune system function," says Dr. Daniel Winer, who is also Assistant Professor, Department of Laboratory Medicine and Pathobiology at University of Toronto.
"Our work characterizes the role of this signaling pathway in immune cells, mainly T cells, opening up avenues in the future to better regulate the immune system."
Although much work has been done in past years on the role of insulin in organs such as the liver, muscle and in fat to understand regulation of glucose or blood sugar and how the body metabolizes or turns it into energy, little is known about how insulin impacts the immune system.
"The link between insulin and the immune system is not obvious," says Dr. Tsai, "it is fascinating to learn that immune cells, which require energy and nutrients for proper functioning just like all other cells in the body, are also regulated by metabolic signals from insulin."
