Journal
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
Volume 60, Issue 1, Pages 1-16Publisher
HUMANA PRESS INC
DOI: 10.1007/s12016-020-08816-3
Keywords
Neutrophils; Neutrophil extracellular traps; Low-density granulocytes; Rheumatic diseases; Autoimmunity
Categories
Funding
- National Natural Science Foundation of China [81971521]
- Peking University People's Hospital Research and Development Fund [RDY2019-14]
- Intramural Research Program at NIAMS/NIH [ZIAAR041199]
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Neutrophils contribute to the initiation, promotion, and perpetuation of immune dysregulation in systemic rheumatic diseases, making them potential targets for therapeutic interventions to improve clinical outcomes.
Systemic rheumatic diseases are a heterogeneous group of disorders characterized by profound immune dysregulation. Recent discoveries have led to a significant resurgence of interest in neutrophils as shapers of immune dysregulation and as triggers of organ damage in rheumatic diseases. Neutrophils contribute to the initiation, promotion, and perpetuation of immune dysregulation through a variety of mechanisms including synthesis of proinflammatory cytokines, direct tissue damage through degranulation and synthesis of reactive oxygen species, and the formation of neutrophil extracellular traps (NETs). The identification of a subset of proinflammatory neutrophils, the low-density granulocytes (LDGs), which promote Th1 responses and cause endothelial dysfunction, has further strengthened the pathogenic role of neutrophils in various rheumatic diseases. The presence of autoantibodies targeting molecules commonly expressed in neutrophils suggests that neutrophils, particularly NETs, may be a source of autoantigens. An imbalance between NET formation and degradation, which leads to increased NET levels in the circulation and tissues, could enhance the exposure of the immune system to modified autoantigens, promote vascular disease, and increase tissue damage. This review will present an overview of recent advances in our understanding of how neutrophil dysregulation modulates the innate and adaptive immune responses in systemic rheumatic diseases and their putative contributions to pathogenicity. Understanding the potential pathogenic role of neutrophil dysregulation may provide better molecular candidates for therapeutic targeting, and ultimately promote improvements in the clinical outcomes in rheumatic diseases.
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