Abstract
Innate immunity includes a cellular and a humoral arm. Long pentraxin 3 (PTX3) is a fluid phase pattern recognition molecule and a key component of the humoral arm of innate immunity. PTX3 is normally produced in response to microbial recognition or inflammatory signals by different immune or stromal cells. In the early phase of skin wound healing, Pentraxin 3 (PTX3)- deficiency was associated with increased fibrin deposition and persistence, and thicker clots. At later phases, increased collagen deposition was observed in Ptx3-deficient mice. A similar phenotype was observed after liver injury. Ptx3-deficient macrophages and fibroblasts showed defective pericellular fibrinolysis in vitro. PTX3 bound fibrinogen/fibrin and plasminogen at acidic pH. The second exon-encoded N-terminal domain of PTX3 recapitulated the interactions observed with the whole molecule. Thus, a prototypic component of humoral innate immunity, PTX3, plays a non-redundant role in the orchestration of tissue repair and remodeling. We suggest that matrix and microbial recognition are commune, ancestral features of the humoral arm of innate immunity.
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