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Cited by 274

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages.

Open access
Lagasse, E, Weissman, I L·1994·The Journal of experimental medicine

Abstract

Neutrophils, the most common inflammatory leukocytes, have the most limited life span of all blood cells. After they undergo apoptosis, they are recognized and engulfed by macrophages. bcl-2, a proto-oncogene rearranged and deregulated in B cell lymphomas bearing the t(14;18) translocation, is known to inhibit programmed death. bcl-2 expression is localized in early myeloid cells of the bone marrow but is absent in mature neutrophils. Transgenic mice that expressed bcl-2 in mature neutrophils showed that bcl-2 blocked neutrophil apoptosis. Despite this, homeostasis of neutrophil population is essentially unaffected. In fact, macrophage uptake of neutrophils expressing bcl-2 still occurred. This transgenic model indicates that the mechanism that triggers phagocytosis of aging neutrophils operates independently of the process of apoptosis regulated by bcl-2.

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Metadata

Authors
Lagasse, E., & Weissman, I. L.
Venue
The Journal of experimental medicine
Published
1994-03-01
Volume
179
Issue
3
Pages
1047-1052
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2164753589
Cited by
274
References
3
FWCI
6.50
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages. https://app.cochat.ai/papers/10.1084/jem.179.3.1047
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Lagasse, E., & Weissman, I. L. (1994). bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages. The Journal of experimental medicine. https://doi.org/10.1084/jem.179.3.1047

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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.