The DOI matches its Crossref record; 110 of the 110 references it cites were found in a registry or an index.
Neutrophil apoptosis pathways and their modifications in inflammation
Abstract
Summary: Neutrophils are constantly produced in large numbers in the bone marrow, and the same numbers of cells need to die within a defined time period in order to keep cellular homeostasis under physiologic conditions. Changing the rate of apoptosis rapidly changes cell numbers in such systems. For instance, in many bacterial and autoimmune inflammatory diseases, delayed apoptosis is one important mechanism for neutrophil accumulation. Excessive production of granulocyte/macrophage colony‐stimulating factor (GM‐CSF) and granulocyte colony‐stimulating factor (G‐CSF), two important neutrophil survival factors, is often observed in such inflammatory responses. Cytokine withdrawal, as it occurs in the resolution phase of inflammation, leads to the induction of apoptosis. Moreover, neutrophil apoptosis can be accelerated both in the presence and in the absence of survival factors by activation of distinct members of the tumor necrosis factor/nerve growth factor receptor family. This review focuses on recently published work regarding signaling pathways that regulate neutrophil apoptosis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Death Receptors: Signaling and Modulation
Ashkenazi, A., & Dixit, V. M. (1998) · Science · doi:10.1126/science.281.5381.1305 · Cited by 5,866
Hengartner, M. O. (2000) · Nature · doi:10.1038/35037710 · Cited by 5,779
The phosphoinositide 3-kinase pathway
Cantley, L. C. (2002) · Science · doi:10.1126/science.296.5573.1655 · Cited by 5,621
Mammalian MAP kinase signalling cascades
Chang, L., & Karin, M. (2001) · Nature · doi:10.1038/35065000 · Cited by 5,111
Regulation of Cell Death Protease Caspase-9 by Phosphorylation
Cardone, M. H., Roy, N., Stennicke, H. R., Salvesen, G. S., Franke, T. F., Stanbridge, E., Frisch, S., & Reed, J. C. (1998) · Science · doi:10.1126/science.282.5392.1318 · Cited by 2,481
IAP proteins: blocking the road to death's door
Salvesen, G. S., & Duckett, C. S. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm830 · Cited by 1,756
Inside the Neutrophil Phagosome: Oxidants, Myeloperoxidase, and Bacterial Killing
Hampton, M. B., Kettle, A. J., & Winterbourn, C. C. (1998) · Blood · doi:10.1182/blood.v92.9.3007 · Cited by 1,652
A blast from the past: clearance of apoptotic cells regulates immune responses
Savill, J., Dransfield, I., Gregory, C., & Haslett, C. (2002) · Nature Reviews Immunology · doi:10.1038/nri957 · Cited by 1,574
Corpse clearance defines the meaning of cell death
Savill, J., & Fadok, V. (2000) · Nature · doi:10.1038/35037722 · Cited by 1,547
Granules of the Human Neutrophilic Polymorphonuclear Leukocyte
Borregaard, N., & Cowland, J. B. (1997) · Blood · doi:10.1182/blood.v89.10.3503 · Cited by 1,522
Cited by
Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis
Yousefi, S., Perozzo, R., Schmid, I., Ziemiecki, A., Schaffner, T., Scapozza, L., Brunner, T., & Simon, H.-U. (2006) · Nature Cell Biology · doi:10.1038/ncb1482 · Cited by 1,158
Self-citationViable neutrophils release mitochondrial DNA to form neutrophil extracellular traps
Yousefi, S., Mihalache, C., Kozlowski, E., Schmid, I., & Simon, H. U. (2009) · Cell Death & Differentiation · doi:10.1038/cdd.2009.96 · Cited by 1,036
Self-citationBours, M. J. L., Swennen, E. L. R., Di Virgilio, F., Cronstein, B. N., & Dagnelie, P. C. (2006) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2005.04.013 · Cited by 1,030
Clearance of apoptotic neutrophils and resolution of inflammation
Greenlee‐Wacker, M. C. (2016) · Immunological Reviews · doi:10.1111/imr.12453 · Cited by 478
Neutrophil Apoptosis: Relevance to the Innate Immune Response and Inflammatory Disease
Fox, S., Leitch, A. E., Duffin, R., Haslett, C., & Rossi, A. G. (2010) · Journal of Innate Immunity · doi:10.1159/000284367 · Cited by 441
Metadata
- Authors
- Simon, H.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2003-05-12
- Volume
- 193
- Issue
- 1
- Pages
- 101-110
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2011670785
- Cited by
- 347
- References
- 110
- FWCI
- 1.59
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Neutrophil apoptosis pathways and their modifications in inflammation. https://app.cochat.ai/papers/10.1034/j.1600-065x.2003.00038.x
- The paper
- Simon, H. (2003). Neutrophil apoptosis pathways and their modifications in inflammation. Immunological Reviews. https://doi.org/10.1034/j.1600-065x.2003.00038.x
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
