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Defining the Role of Type I Interferon Signaling in the Increased Accumulation of Versican in Lungs of Mice Exposed to Influenza Infection

The accumulation of versican in the extracellular matrix (ECM) has been described as part of the innate immune response to viral lung infection. However, the mechanism(s) regulating versican expression during influenza infection are not understood. Previous work has identified both the β‐catenin/T‐cell factor pathway and the TLR/Trif/Type I interferon (IFN) receptor pathway as controlling versican expression in stromal cells and macrophages respectively. The goal of this study, is to investigate the role of Type I IFN receptor signaling in directing versican accumulation in the lungs during influenza infection.