Characterisation of a novel non-canonical interferon pathway and its implications in inflammatory disease

Type I interferon (IFN) signaling is essential in the protection against viral infection and cancer growth. However, excessive activation can lead to the development of autoimmune diseases such as systemic lupus erythematosus. Recently, our lab has discovered a novel IFN axis, where activation in mouse models of sepsis leads to lethality. The blockade of this novel pathway was shown to rescue these mice from fatality. This thesis identifies the cell types and tissues with the potential to activate this inflammatory pathway. It also develops a powerful microscopy method to visualise molecular interactions of this new axis at the cell surface.