As scientists continue studying type 1 diabetes (T1D), they develop a deeper understanding of changes that occur in the body. It has been known for a while that the body attacks insulin-producing beta cells in the pancreas leaving the body unable to regulate blood sugar. Researchers have recently discovered that MAIT cells within the body – cells that are activated by bacteria and associated with mucosae – may also play a role. They are part of the body’s innate immune system and may serve as a biomarker for early detection of T1D.
The study, which was conducted by AP-HP Necker-Enfants Malades Hospital in Paris and the Cochin Institute, examined blood sample from patients with and without T1D, as well as animal models. The results showed that MAIT cell levels were lower in the blood of children diagnosed with T1D than those who were not. This could be because the MAIT cells had migrated to the pancreas in children with T1D; they are believed to play a role in the destruction of insulin-producing beta cells. But one interesting point to note was that before T1D had even developed in the animal models, the MAIT cells were already altered. This could serve as an early form of detection and prevention of the disease.
The mutation in MAIT cells may also contribute to gut mucosa being more susceptible to bacteria. This may lead to an increased autoimmune response. When MAIT cells are functioning normally, they help maintain homeostasis in the gut mucosa.
Scientists may be able to use this information to enhance early detection of T1D, develop strategies for prevention, or improve targeted treatment options. More research is needed to explore the link between MAIT cells and gut microbiota, but this is a starting point.
The Diabetes Research Connection actively supports novel research regarding preventing, treating, and potentially curing T1D. The organization raises funds that are provided to early career scientists for innovative research projects. To learn more and support their efforts, visit http://diabetesresearchconnection.org.