Ptx3, also known as long pentraxin 3, is a soluble pattern recognition molecule belonging to the humoral innate immune system. It rapidly produced at inflammatory sites by phagocytes and stromal cells in response to infection or tissue injury. PTX3 interacts with microbial moieties, pathogens, molecules of the complement and hemostatic systems, and extracellular matrix components, playing a crucial role in innate immunity, inflammation, and matrix remodeling [1].

In mice, PTX3-deficiency was associated with worsening of idiopathic pulmonary fibrosis (IPF), impaired fibrin removal, and increased collagen deposition, suggesting its protective role in IPF [1]. Ptx3-targeted mice exhibit reduced trabecular volume during bone development and impaired callus mineralization following experimental fracture, indicating its role in bone homeostasis [2]. In the context of hepatic ischemia-reperfusion injury, macrophages with high PTX3 expression exhibit M1-like characteristics, and PTX3 knockdown reduces hepatocyte pyroptosis, demonstrating its role in regulating macrophage-mediated inflammation [3]. Ptx3-deficient mice also show lymphatic vessel (LV) abnormalities in the colon submucosa and diaphragm, defective fluid drainage, and defective dendritic cell trafficking, revealing its importance in LV structural organization and immunological function [4].

In conclusion, Ptx3 is essential for multiple biological processes such as innate immunity, tissue repair, bone homeostasis, and lymphatic system function. Studies using Ptx3-deficient mouse models have provided valuable insights into its role in diseases like IPF, highlighting its potential as a therapeutic target in these disease areas.