Neutrophil-derived proteinase 3 induces kallikrein-independent release of a novel vasoactive kinin.


The kinin-forming pathway is activated on endothelial cells and neutrophils when high-molecular weight kininogen (HK) is cleaved by plasma kallikrein liberating bradykinin, a potent mediator of inflammation. Kinins are released during inflammatory conditions such as vasculitis, associated with neutrophil influx around blood vessels. Some patients with… (More)
DOI: 10.4049/jimmunol.0803624

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