Objectives of the Project
We have previously seen that reduced ability of neutrophils to produce reactive oxygen species (ROS) is associated with increased severity and organ damage in SLE. This prompted us to ask if SLE patients are genetically predisposed to have low ROS production and how this would influence pathogenesis. We are investigating the role of NCF1 gene variants in SLE and relate this to disease phenotypes. We are also characterizing the role of ROS and neutrophils in regulation of key immunopathogenic events in SLE, focusing on NETosis, type I interferon production and activation of adaptive immunity.