Abstract
Introduction: Deep vein thrombosis (DVT) resolution occurs via an inflammatory response. As most DVT are sterile, endogenous danger signals, such as nucleic or uric acids, must incite the inflammatory response. Neutrophils and monocyte/macrophages are important in DVT resolution; the role of dendritic cells is not well defined. Toll-like receptor 9 (TLR9) is expressed on these cells and activation by foreign or endogenous nucleic acids triggers an innate immune response. Previously, we have shown that loss of TLR9 signaling is associated with impaired venous thrombosis (VT) resolution and increased necrotic cell products in mice.
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