An ounce of prevention is worth a pound of cure, as the adage goes. At Helmsley, we strive to support pioneering research aiming to prevent or delay the development of type 1 diabetes (T1D) because we know that this strategy could significantly improve long term health outcomes for those at risk of developing the condition. To make novel interventions that change the course of the disease a reality, more research is necessary into the mechanisms that cause it in the first place. That’s why Helmsley’s Type 1 Diabetes Program has issued a request for proposals (RFP) to support innovative research coming at the problem from a new angle: investigating the role of innate immunity during the development of T1D.
Autoimmune diseases are characterized by the immune system mistakenly targeting and damaging parts of the body. In T1D, the target is pancreatic beta cells, which produce insulin. This leads to subsequent inability to regulate blood sugar levels and long-term health consequences. The human immune system, which protects people from infections, is composed of innate and adaptive immune responses. The innate immune system is a less specific first line of defense and includes physical barriers, like skin and mucus membranes, cells, and inflammatory pathways. Innate immunity acts quickly to eliminate the infection but cannot prevent reinfection. The adaptive immune system, in contrast, initiates later in the infection, recognizes specific pathogens through cells or proteins like antibodies, and provides an immune memory so we’re better prepared if we face the same pathogen again.
The vast majority of research to date on immunology in T1D has focused on the adaptive immune response. For example, researchers have demonstrated that T cells, part of the adaptive immune system, play a crucial role in mediating the development of T1D by attacking beta cells. While researchers continue to explore how beta cells are damaged by T cells, there is a growing body of evidence that the innate immune system also plays a role in the development of T1D. Innate immune cells, like macrophages, infiltrate the pancreas during the onset of T1D, producing inflammatory substances that may influence the activation of T cells and the continued attack on beta cells in early stage T1D. These cells might also contribute in the recruitment of T cells to the beta cells, or even dampen immune responses. But not enough is known about the contributions of the innate immune system in the context of T1D.
Assessing the whole immune environment that contributes to the development of T1D is critical to identifying novel therapeutics that could prevent or delay the onset of T1D in at-risk individuals. We look to facilitate this by supporting researchers to understand and target the understudied innate immune system in T1D pathogenesis through this RFP. Together we can move the field closer to better prevention strategies for this challenging disease.