Constitutive Neutrophil Apoptosis: Mechanisms and Regulation

DSpace/Manakin Repository

Constitutive Neutrophil Apoptosis: Mechanisms and Regulation

Citable link to this page


Title: Constitutive Neutrophil Apoptosis: Mechanisms and Regulation
Author: Luo, Hongbo; Loison, Fabien

Note: Order does not necessarily reflect citation order of authors.

Citation: Luo, Hongbo R., and Fabien Loison. 2008. “Constitutive Neutrophil Apoptosis: Mechanisms and Regulation.” American Journal of Hematology 83 (4) (April): 288–295. doi:10.1002/ajh.21078.
Access Status: Full text of the requested work is not available in DASH at this time (“dark deposit”). For more information on dark deposits, see our FAQ.
Full Text & Related Files:
Abstract: Neutrophil constitutive death is a critical cellular process for modulating neutrophil number and function, and it plays an essential role in neutrophil homeostasis and the resolution of inflammation. Neutrophils die due to programmed cell death or apoptosis. In this article, we review recent studies on the mechanism of neutrophil apoptosis. The involvement of caspase, calpain, reactive oxygen species, cellular survival/death signaling pathways, mitochondria, and BCL-2 family member proteins are discussed. The fate of neutrophils can be influenced within the inflammatory microenvironment. We summarize the current understanding regarding the modulation of neutrophil apoptotic death by various extracellular stimuli such as proinflammatory cytokines, cell adhesion, phagocytosis, red blood cells, and platelets. The involvement of neutrophil apoptosis in infectious and inflammatory diseases is also addressed.
Published Version: doi:10.1002/ajh.21078
Other Sources:
Citable link to this page:
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)


Search DASH

Advanced Search