Neutrophils account for almost 50–70% of all circulating leukocytes in human blood and are important effector cells in the innate and adaptive immune response.1,2 Neutrophils, once released from the bone marrow to the blood circulation, can be mobilized to sites of infection or inflammation through the leukocyte adhesion cascade. In case of infection, neutrophils function as pathogen killers by destroying invading pathogens through phagocytosis, degranulation, and release of nuclear material in form of NETs.1

Once recruited to the site of inflammation, neutrophils can undergo phenotypic changes and generate various subpopulations with various cellular functions.1 Neutrophils regulate the maturation of dendritic cells (DCs) to effective APCs, regulate macrophage and T-cell activity, stimulate B-cell and NK-cell maturation, and contribute to barrier function regulation by interacting with endothelial and epithelial cells.2,3 Reciprocally, neutrophil activity can also be modulated by elements of the adaptive immune system – for instance, DCs can inhibit generation and function of neutrophils.3

Several neutrophil products, like lactoferrin, α-defensins, and chemokines are essential for neutrophil-DC interaction. Neutrophils produce BAFF and APRIL, which are required for B-cell survival and activation. Granule proteins (eg, S100A and antimicrobial peptides) and chemokines produced by neutrophils contribute to monocyte influx at inflammation sites.2

Absolute neutrophil count (ANC) is considered one of the important inflammatory markers in several disease settings.4,5

APC: antigen-presenting cell; APRIL: a proliferation-inducing ligand; BAFF: B-cell activating factor; NET: neutrophil extracellular trap; NK: natural killer.


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    Nauseef WM, Borregaard N. Nat Immunol. 2014;15:602-611.

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    Mahende C, Ngasala B, Lushingu J, et al. Pan Afr Med J. 2017;26:51.

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    Zhu X, Chen Y, Cui Y. Dis Markers. 2020;2020:1371964.