Researchers at the ULB Center for Diabetes Research have uncovered a possible mechanism of pancreatic β cell destruction in type 1 diabetes (T1D). Gene expression analyses revealed a different induction of cell autonomous immune responses in α and β cells. The higher susceptibility of β cells to viral infection potentially explains why these cells are targeted by the immune system in T1D.
Type 1 diabetes is an autoimmune disease in which the insulin producing β cells of the pancreas are destroyed while other islet cells remain unharmed. Thanks to the effort of the ULB Center for Diabetes, the reasons as to why specifically these cells are lost have become a bit clearer.
While genetics contribute to T1D susceptibility, environmental factors, such as infection with the coxsackievirus, can also play a significant role. When rat pancreatic α and β cells are exposed to coxsackievirus, α cells boost gene expression for virus clearance to a greater extent than β cells. Induction of these IFN- and STAT1-regulated genes mounts an effective defense against the infecting virus. As initial infection isn't resolved in β cells, a persistent low level infection can cause chronic inflammation and recruitment of immune cells. It is believed that this differential ability to clear viral infections is a cause of selective β cell loss in T1D.
The understanding of this cell autonomous immunity might offer insights on how to protect β cells from viral infection and can aid in lowering the risk for the development of T1D.
Marroqui, Laura, et al. "Differential cell autonomous responses determine the outcome of coxsackievirus infections in murine pancreatic α and β cells." Elife4 (2015): e06990.