IMR Press / FBL / Volume 13 / Issue 14 / DOI: 10.2741/3099

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Control of granule exocytosis in neutrophils
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1 Pulmonary Research Group, Department of Medicine, Edmonton, Canada
2 Department of Cell Biology, University of Alberta, Edmonton, Canada
Academic Editor:Oliver Soehnlein
Front. Biosci. (Landmark Ed) 2008, 13(14), 5559–5570; https://doi.org/10.2741/3099
Published: 1 May 2008
Abstract

Neutrophils are granulocytes derived from bone marrow that circulate through the blood and become recruited to tissues during infection or inflammation. They are the most abundant white blood cell and comprise the first line of defence in the innate immune system. However, they are also capable of causing tissue damage in a wide range of diseases. Release of chemotactic signals from inflamed or infected tissues trigger neutrophil migration from the bloodstream to inflammatory foci, where they contribute to inflammation by undergoing receptor-mediated respiratory burst and degranulation. Degranulation from neutrophils has been implicated as a major causative factor in numerous inflammatory diseases. However, the mechanisms that control neutrophil degranulation are not well understood. Recent observations indicate that receptor-mediated granule release from neutrophils depends on activation of distal signaling pathways that include the src family of tyrosine kinases, β-arrestins, the tyrosine phosphatase MEG2, the kinase MARCK, Rabs and SNAREs, and the Rho GTPase, Rac2. Some of these pathways are specifically required for membrane fusion between the granule and plasma membrane, leading to exocytosis. This review focuses on the understanding of distal molecular mechanisms controlling exocytosis from neutrophils.

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