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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWCathepsin G inhibitor I is an inhibitor of cathepsin G (IC50 = 53 nM).1 It is selective for cathepsin G over various serine proteases, including thrombin, Factor Xa, Factor IXa, plasmin, trypsin, and leukocyte proteinase 3 (PR3; IC50s = >100 µM for all), but also weakly inhibits chymotrypsin. It inhibits cathepsin G-induced activation of IL-36 in neutrophil degranulates when used at a concentration of 10 µM.2 Cathepsin G inhibitor I (10 µM) reduces CD4+ T cell-induced secretion of IFN-γ and IL-17 in B cells incubated with tetanus toxin C-fragments (TTC) and also reduces TTC presentation in B cells.3 It decreases the size of neuromyelitis optica lesions and reduces the number of perivascular neutrophils, indicating decreased neutrophil brain entry, when used in combination with the neutrophil elastase inhibitor sivelestat (Item No. 17779) in a mouse model of IgG-induced brain injury when administered intracerebrally at a dose of 5 µg/animal.4
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1. Nonpeptide inhibitors of cathepsin G: Optimization of a novel β-
2. Neutrophil-
3. Application of specific cell permeable cathepsin G inhibitors resulted in reduced antigen processing in primary dendritic cells. Mol. Immunol. 46(15), 2994-2999 (2009).
4. Neutrophil protease inhibition reduces neuromyelitis optica-
Cathepsin C promotes breast cancer lung metastasis by modulating neutrophil infiltration and neutrophil extracellular trap formation. Cancer Cell 39(3), 423-437 (2021).