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Abstract
Objective The objective of this review is to highlight the role of Neutrophil Extracellular Traps (NETs) in the pathogenesis of Systemic Lupus Erythematosus (SLE), focusing on their development, composition, and contribution to autoimmune processes.
Methods In this research, we performed an analysis of the existing literature to gather comprehensive insights into the involvement of NETs in SLE. We reviewed studies on NET formation mechanisms, their composition, and their role in autoimmune responses. Furthermore, we explored the influence of NETs in thrombosis and autoimmune diseases, thereby focusing on SLE.
Results Neutrophils and other leucocytes release NETs as a part of the innate immune response. These web-like structures consist of decondensed chromatin decorated with various antimicrobial proteins. While NETs play a crucial role in pathogen clearance, they have been involved in the development and pathogenesis of autoimmune diseases, including SLE. NETs contribute to SLE by releasing nuclear antigens into the extracellular space and promoting the production of autoantibodies against self-antigens.
NET formation in SLE is facilitated by mechanisms involving neutrophil activation and their subsequent release of chromatin into the extracellular space. NETs serve as a source of autoantigens, triggering an autoimmune response that is characterized by the production of autoantibodies against nuclear antigens such as double-stranded DNA. NETs also interact with B cells and dendritic cells, thereby further amplifying the autoimmune response (see figure 1).
In addition to their role in autoimmunity, NETs involved in immunothrombosis, a process where the innate immune system leads to pathological thrombosis. Aggregated extracellular chromatin can activate blood platelets, promote thrombus development, and contribute to occlusion of blood vessels. Additionally, NETs can modify immune responses by their activation of the coagulation cascade, the inflammasome, and the complement system.
Conclusion Neutrophil Extracellular Traps (NETs) play multiple roles in the pathogenesis of Systemic Lupus Erythematosus (SLE). Even though NETs are essential for pathogen clearance, their dysregulation contributes to the release of self-antigens and triggers the production of autoantibodies against nuclear constituents. NETs also contribute to immunothrombosis leading to vessel occlusion and damage to multiple organs in SLE. Understanding the complicated involvement of NETs in SLE pathogenesis opens promising ways for therapeutic interventions focused at regulating NET release and degradation. This research emphasizes the importance of further research on the mechanisms underlying NET formation and their involvement in SLE, ultimately paving the way for novel therapeutic strategies in autoimmune diseases.
Funding No external funding.
Pathomechanisms of neutrophil extracellular traps (NETs) contributing to SLE
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