Anti-type I interferon (IFN) autoantibodies (aAbs) bind to IFN and prevent them from establishing a robust innate immune response. Individuals with anti-IFN aAbs are at increased risk of severe infections.
Currently the exact mechanisms behind the development of these autoantibodies remain unclear. In this study we will aim to isolate and sequence the B cells for producing anti-IFN aAbs and to identify common genetic markers. By targeting these markers with immunotherapy (for deletion), we hope to reduce the risk of severe disease in affected individuals. This research could pave the way for new treatments that enhance immune response and protect against serious disease.