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Cited by 263

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Caspase-8 is activated by cathepsin D initiating neutrophil apoptosis during the resolution of inflammation

Open access
Conus, Sébastien, Perozzo, Remo, Reinheckel, Thomas, Peters, Christoph, Scapozza, Leonardo, Yousefi, Shida, Simon, Hans-Uwe·2008·The Journal of Experimental Medicine

Abstract

In the resolution of inflammatory responses, neutrophils rapidly undergo apoptosis. We describe a new proapoptotic pathway in which cathepsin D directly activates caspase-8. Cathepsin D is released from azurophilic granules in neutrophils in a caspase-independent but reactive oxygen species–dependent manner. Under inflammatory conditions, the translocation of cathepsin D in the cytosol is blocked. Pharmacological or genetic inhibition of cathepsin D resulted in delayed caspase activation and reduced neutrophil apoptosis. Cathepsin D deficiency or lack of its translocation in the cytosol prolongs innate immune responses in experimental bacterial infection and in septic shock. Thus, we identified a new function of azurophilic granules that is in addition to their role in bacterial defense mechanisms: to regulate the life span of neutrophils and, therefore, the duration of innate immune responses through the release of cathepsin D.

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Crossref · 10.1084/jem.20072152

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Metadata

Authors
Conus, S., Perozzo, R., Reinheckel, T., Peters, C., Scapozza, L., Yousefi, S., & Simon, H.-U.
Venue
The Journal of Experimental Medicine
Published
2008-02-25
Volume
205
Issue
3
Pages
685-698
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2115999682
Cited by
263
References
4
FWCI
9.93
Type
journal article
Language
en
Open access
green

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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