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During the active remyelinating phase, both CysF knockdown (CysFKD) and microglial-selective CatC overexpression (CatCOE) showed a worsening of the demyelination in Plp(4e/-) transgenic mice. Conversely, during the chronic demyelinating phase, CatC knockdown (CatCKD) ameliorated the demyelination. Our results suggest that the balance between CatC and CysF expression controls the demyelination and remyelination process.
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Neutrophilic Cathepsin C Is Maturated by a Multistep Proteolytic Process and Secreted by Activated Cells during Inflammatory Lung Diseases.
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A proteolytic cascade, involving cathepsins C and D, controls LLOMe-mediated necrosis.
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Double immunofluorescence analysis showed that CTLA-2alpha was co-localized with cathepsin L, cathepsin C, and TINAGL1 in placenta.
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CatC has a role in the selective tuning of innate and adaptive immune responses, relevant to a chronic immune disease, such as atherosclerosis.
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Data indicate that all-trans retinoic acid (ATRA), which induces miR-23a expression, decreases cathepsin C (CTSC) expression and granzyme B activity leading to impaired NK cell cytotoxicity.
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These results establish that DPPI is a major determinant of survival following Klebsiella pneumoniae lung infection and suggest that the survival disadvantage in DPPI(+/+) mice is in part due to processing of surfactant protein D by DPPI.
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found no significant role for CtsC during mammary carcinogenesis but revealed squamous carcinogenesis to be functionally dependent on CtsC
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Late stage cathepsin C, CXCL13 and Ki-67 overexpression correlate with regional neuropathology in a bovine spongiform encephalopathy transgenic murine model.
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Proinflammatory cytokines induce expression and release of cathepsin C in microglial cells during neuroinflammatory progression.
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The production of IL-1beta by macrophages, neutrophils, and mast cells in vitro is dependent on caspase-1 but not on cathepsin C.
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NADPH oxidase in antimicrobial host defense against A. fumigatus and B. cepacia, whereas the proteases neutrophil elastase, cathepsin G, and lysosomal cysteine protease cathepsin C/ dipeptidyl peptidase I are dispensable
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CatC is involved in limiting MCMV replication; however, this effect is independent of its role in promoting effector cytolytic activity.
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Results indicate that mast cell dipeptidyl peptidase I (DPPI) harms the septic host and that DPPI is a novel potential therapeutic target for treatment of sepsis.
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DPPI regulates a critical step in the development of collagen-induced arthritis that is independent of T cell and B cell functions.
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Overall, our results indicate that although cathepsin C clearly generates the majority of granzyme B activity, some is still generated in its absence, pointing to alternative mechanisms for granzyme B processing and activation.
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These findings suggest that DPPI and/or granule-associated serine proteases are necessary for neutrophil recruitment into the diseased aorta and that these proteases act to amplify vascular wall inflammation that leads to abdominal aortic aneurysms.
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Role of DPPI and TIMP-3 in development of pulmonary fibrosis in early inflammation following bleomycin instillation.
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DPPI is involved in recruitment of neutrophils following respiratory viral infection; absence of neutrophil-derived DPPI diminishes the acute inflammatory response and mucous cell metaplasia of the chronic asthma that follows Sendai virus infection.
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Results indicate that DPPI cannot functionally compensate for the loss of TPPI.