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Toronto General Hospital Research Institute (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 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.
In their previous work, researchers demonstrated that immune cells inside abdominal fat cause the release of ‘pro-inflammatory’ chemicals, which make the body less sensitive to insulin. Obesity is linked to whole body insulin resistance, and obese insulin-resistant individuals and mice are known to have weakened immune responses, and increased susceptibility to developing severe infections.
There is a link between persistent and chronic inflammation, immune dysfunction and insulin resistance, with the end result that T cells stop responding and become functionally impaired. The study shows how insulin regulates T cell function and what causes T cells to stop responding to insulin. Using genetically engineered mice, the research team designed mice with T cells that did not have an insulin receptor on them, mimicking insulin resistance. Then observed what happened to the T cells in the mice under different stressors, such as the H1N1 flu virus.
T cells need more signals to boost their activation after they encounter a foreign invader, insulin receptor or signaling molecule is like a second push to the immune system to ensure that it can fight off the infection with the best weapons it has. Without the added boost or kickstart provided by the insulin receptor to re-energize the T cells to mount an effective immune response, the T cells failed to destroy viruses such as the H1N1 influenza