Neutrophils are the most abundant circulating leukocytes and form the first immune defense line against bacterial and fungal infections. Dysregulation in the function and phenotype of neutrophils also play important roles in the pathogenesis of a wide range of autoimmune and autoinflammatory diseases. Neutrophils secrete granules full of cytotoxic enzymes, produce ROS and various antimicrobial peptides and form neutrophil extracellular traps (NETs), therefore contributing to tissue damage and initiating local or systemic immune response.
As effector cells of the innate immune system, neutrophils function in a multitude of ways to direct the inflammatory response. Activated neutrophils produce a number antimicrobial peptides that regulate both pro- and anti-inflammatory responses, release large amount of ROS and proteases extracellularly, which result in damage to host tissues, modification of host proteins, lipids and DNA and dysregulation of oxidative homeostasis. Neutrophil-derived NETs could serve as self-autoantigens (DNA, citrullinated histones or proteinase 3) that trigger a strong adaptive immune response in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). In addition, neutrophils and NETs regulate the function of innate (ILC, DC, et al.) and adaptive cells (ILC) during autoimmune response. Given that the neutrophils are more generally involved in host homeostasis than previously thought, detailed functions and roles of neutrophils and NETs in autoimmune and autoinflammatory diseases need to be further investigated.
In this Research Topic, we aim to provide a forum for cutting-edge research to describe the roles of neutrophils and NETs in autoimmune and autoinflammatory diseases (such as psoriasis, SLE, inflammatory bowel disease (IBD), RA) and explore innovative therapeutic approaches to target neutrophils.
We welcome the submissions of Original Research and Review that cover, but are not limited to, the following sub-topics:
1) Role and mechanisms of neutrophils and NETs in autoimmune and autoinflammatory diseases.
2) Modulation of neutrophil heterogeneity in autoimmune and autoinflammatory diseases.
3) Mechanisms of abnormal neutrophil adhesion and migration in autoimmune and autoinflammatory diseases.
4) Interaction between neutrophil and immune cells or non-immune cells.
5) Functions and mechanisms of reverse transmigration of neutrophils.
6) New therapeutic strategy targeting neutrophils and NETs.
Neutrophils are the most abundant circulating leukocytes and form the first immune defense line against bacterial and fungal infections. Dysregulation in the function and phenotype of neutrophils also play important roles in the pathogenesis of a wide range of autoimmune and autoinflammatory diseases. Neutrophils secrete granules full of cytotoxic enzymes, produce ROS and various antimicrobial peptides and form neutrophil extracellular traps (NETs), therefore contributing to tissue damage and initiating local or systemic immune response.
As effector cells of the innate immune system, neutrophils function in a multitude of ways to direct the inflammatory response. Activated neutrophils produce a number antimicrobial peptides that regulate both pro- and anti-inflammatory responses, release large amount of ROS and proteases extracellularly, which result in damage to host tissues, modification of host proteins, lipids and DNA and dysregulation of oxidative homeostasis. Neutrophil-derived NETs could serve as self-autoantigens (DNA, citrullinated histones or proteinase 3) that trigger a strong adaptive immune response in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). In addition, neutrophils and NETs regulate the function of innate (ILC, DC, et al.) and adaptive cells (ILC) during autoimmune response. Given that the neutrophils are more generally involved in host homeostasis than previously thought, detailed functions and roles of neutrophils and NETs in autoimmune and autoinflammatory diseases need to be further investigated.
In this Research Topic, we aim to provide a forum for cutting-edge research to describe the roles of neutrophils and NETs in autoimmune and autoinflammatory diseases (such as psoriasis, SLE, inflammatory bowel disease (IBD), RA) and explore innovative therapeutic approaches to target neutrophils.
We welcome the submissions of Original Research and Review that cover, but are not limited to, the following sub-topics:
1) Role and mechanisms of neutrophils and NETs in autoimmune and autoinflammatory diseases.
2) Modulation of neutrophil heterogeneity in autoimmune and autoinflammatory diseases.
3) Mechanisms of abnormal neutrophil adhesion and migration in autoimmune and autoinflammatory diseases.
4) Interaction between neutrophil and immune cells or non-immune cells.
5) Functions and mechanisms of reverse transmigration of neutrophils.
6) New therapeutic strategy targeting neutrophils and NETs.
