The pancreas secretes insulin, a naturally occurring hormone, that is essential for the human body. Individuals with diabetes are prescribed insulin due to non-production or improper use of insulin by the body, known as type 1 and type 2 diabetes respectively. T cells are active participants in our immune response and critical effectors of cell-mediated immunity; they play a pivotal role in self-defense against infections. But what relation does insulin play when it comes to the immune system?
Previous research has focused on the role of insulin in organs such as the liver, or in muscle and fat regulation, but little has been studied on the impact of insulin on the immune system. People with type 2 diabetes who are obese, or those at risk for developing type 2 diabetes, do not respond well or are resistant to insulin. It is also known that obesity linked to insulin resistance in humans and mice results in weakened immune responses and increased susceptibility to developing a severe infection. Two labs, the Winer Labs, demonstrated that immune cells inside abdominal fat stimulate the release of pro-inflammatory chemicals which contributes to the bodies impaired sensitivity to insulin. These results led researchers to study the link between insulin and the immune response further.
A recent study published in Cell Metabolism, by Dr. Sue Tsai, postdoctoral fellow, and senior authors Dr. Daniel Winer, Anatomical Pathologist at University Health Network and Toronto General Hospital Research Institute and Dr. Shawn Winer, Anatomical Pathologist at St. Michael’s Hospital sought to elucidate the insulin and immune system relationship. These researchers wanted to study how insulin regulates T cell function and what causes T cells to stop responding to insulin. The study utilized genetically engineered mice that had T cells lacking an insulin receptor to mimic insulin resistance. The mice were then exposed to different stressors such as the H1N1 influenza virus; researchers observed what effect these stressors had on the insulin resistant T cells.
When fighting infection T cells receive signals to boost their activation when encountering a foreign invader, the insulin receptor on the cell that interacts with a signaling molecule is a second push to bolster the immune response to foreign invaders. When the insulin receptor is non-functional, this boost isn’t present and the T cells fail to destroy viruses such as H1N1 influenza. This specific insulin signaling pathway revs up the immune response when activated by promoting T cell division and secretion of chemical messenger proteins that activate the rest of the immune system.
Future studies will focus on harnessing the insulin signaling pathway to boost the immune response to create vaccines or dampen the reaction in the case of inflammatory illnesses such as arthritis. "T cells are at the heart of so many diseases," says Dr. Tsai, "If we can understand them at the cellular level, this will give us the best opportunity to find new pathways to target for new therapies."
To learn more about diabetes and insulin resistance watch the video below!
Sources: University Health Network, Cell Metabolism, American Diabetes Association