Abstract

Polymorphonuclear neutrophils (PMNs) are traditionally regarded as professional phagocytic and acute inflammatory cells that engulf the microbial pathogens. However, accumulating data have suggested that PMNs are multi-potential cells exhibiting many important biological functions in addition to phagocytosis. These newly found novel activities of PMN include production of different kinds of cytokines/chemokines/growth factors, release of neutrophil extracellular traps (NET)/ectosomes/exosomes and trogocytosis (membrane exchange) with neighboring cells for modulating innate, and adaptive immune responses. Besides, PMNs exhibit potential heterogeneity and plasticity in involving antibody-dependent cellular cytotoxicity (ADCC), cancer immunity, autoimmunity, inflammatory rheumatic diseases, and cardiovascular diseases. Interestingly, PMNs may also play a role in ameliorating inflammatory reaction and wound healing by a subset of PMN myeloid-derived suppressor cells (PMN-MDSC). Furthermore, PMNs can interact with other non-immune cells including platelets, epithelial and endothelial cells to link hemostasis, mucosal inflammation, and atherogenesis. The release of low-density granulocytes (LDG) from bone marrow initiates systemic autoimmune reaction in systemic lupus erythematosus (SLE). In clinical application, identification of certain PMN phenotypes may become prognostic factors for severe traumatic patients. In the present review, we will discuss these newly discovered biological and pathobiological functions of the PMNs.

Highlights

  • Polymorphonuclear neutrophils (PMNs) have long been known as an essential element of the innate immune system, but have been ignored of their participation in the adaptive immune responses or autoimmune reaction

  • The Dark Side of neutrophil extracellular traps (NET): Its Decreased Clearance Induces Autoantibody Production in Several types of NETosis have been reclassified in recent years, such as vital [53], fatal [54,55], and a variety of suicidal NETosis based on the presence of mitochondrial

  • These results have suggested that PMN-derived ectosomes (PMN-Ect) can exert potent antiinflammatory activities in the early stage of inflammation

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Summary

Introduction

Polymorphonuclear neutrophils (PMNs) have long been known as an essential element of the innate immune system, but have been ignored of their participation in the adaptive immune responses or autoimmune reaction. In a series of in vivo studies, Sendo et al [1,2,3] found that depleting PMNs by anti-PMN antibodies in rats led to the abolishment of a number of immune effector functions such as delayed-type hypersensitivity [1], tumor inhibitory activity [2], and antibody-producing capacity [3] These results may suggest that PMN is not merely a terminally differentiated phagocytic cell against bacterial pathogens and an elicitor of acute inflammation, but can actively participate in the immune responses. PMNs are currently considered as complex but enigmatic cells in conducting novel biological functions, including effectors of the innate immune responses, tumor killing, autoimmunity, chronic inflammatory reaction, anti-inflammation, and wound repair [10] In this mini-review, we will discuss in detail the novel biological activities of PMNs in health and disease states consecutively

The Newly Found Biological Functions of PMNs
The Physiology and Molecular Basis of NET Formation
The Dark Side of NET
The Effects of Released Granule Proteins in Modulating Innate and Adaptive
The Extracellular Microvesicles Budding or Extruded from PMNs for Remote
Specific Functions of Ectosomes Extruded from PMNs
Cross-Talk among PMN and Other Immune-Related Cells via Trogocytosis
Neutrophil–Epithelial Interactions
Neutrophil Diversity in Pregnancy
Molecular Mechanisms of Immunosuppression by PMN-MDSC Phenotype
The Roles of PMNs in Inflammation Resolution and Wound Healing
The Role of PMN in Inflammation Extinction in Acute Inflammatory Sites
The Role of PMN on Wound Healing
Role of Neutrophils in Atherogenesis
Conclusions and Prospects
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