Neutrophil extracellular traps (NETs) are unique fibrous structures released by neutrophils in response to various pathogens, exhibiting both anti-inflammatory and proinflammatory effects. In autoimmune conditions, NETs serve as crucial self-antigens triggering inflammatory cascades by activating the inflammasome and complement systems, disrupting self-tolerance mechanisms and accelerating autoimmune responses. Furthermore, NETs play a pivotal role in modulating immune cell activation, affecting adaptive immune responses. This review outlines the intricate relationship between NETs and various diseases, including inflammatory arthritis, systemic autoimmune diseases, Behçet's disease, systemic lupus erythematosus, autoimmune kidney diseases, autoimmune skin conditions, systemic sclerosis, systemic vasculitis, and gouty arthritis. It highlights the potential of targeting NETs as a therapeutic strategy in autoimmune diseases. By examining the dynamic balance between NET formation and clearance in autoimmune conditions, this review offers critical insights and a theoretical foundation for future research on NET-related mechanisms. Advances in systems biology, flow cytometry, and single-cell multiomics sequencing have provided valuable tools for exploring the molecular mechanisms of neutrophils and NETs. These advancements have renewed focus on the role of neutrophils and NETs in autoimmune diseases, offering promising avenues for further investigation into their clinical implications.
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http://dx.doi.org/10.1002/mco2.70101 | DOI Listing |
J Cutan Med Surg
March 2025
Division of Dermatology, University of Alberta, Edmonton, AB, Canada.
Calcinosis cutis, characterized by the pathological deposition of insoluble calcium salts in the skin, is associated with several disease entities, particularly autoimmune conditions such as scleroderma and dermatomyositis. Lesions of calcinosis are often painful, prone to ulceration, and significantly impair quality of life. Despite the clinical impact, no effective treatments have been established to date, making prevention of this condition a critical priority.
View Article and Find Full Text PDFJAMA Dermatol
March 2025
Service de Dermatologie et Allergologie, Faculté de Médecine, Sorbonne Université, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris, Paris, France.
Importance: VEXAS syndrome (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) is a monogenic disease caused by UBA1 somatic variants in hematopoietic progenitor cells, mostly involving adult men. It is associated with inflammatory-related symptoms, frequently involving the skin and hematological disorders. Recently described myelodysplasia cutis (MDS-cutis) is a cutaneous manifestation of myelodysplasia in which clonal myelodysplastic cells infiltrate the skin.
View Article and Find Full Text PDFCells
March 2025
Departement of Rheumatology, Erasme-HUB Hospital, Université Libre de Bruxelles, 1070 Brussels, Belgium.
Tubulointerstitial hypoxia is a key factor for lupus nephritis progression to end-stage renal disease. Numerous aquaporins (AQPs) are expressed by renal tubules and are essential for their proper functioning. The aim of this study is to characterize the tubular expression of AQP1, AQP2 and AQP3, which could provide a better understanding of tubulointerstitial stress during lupus nephritis.
View Article and Find Full Text PDFCells
February 2025
Department of Clinical Internal, Anaesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy.
The thrombotic physiopathology of antiphospholipid syndrome (APS) is complex, heterogeneous, and dynamic. While venous thromboembolism (VTE) is the most common initial presentation, arterial thrombotic events (ATE) become more frequent in advanced stages and are associated with high morbidity and mortality. Despite the use of oral anticoagulants (OACs), thrombotic APS remains associated with a high risk of recurrent thrombosis.
View Article and Find Full Text PDFAltern Ther Health Med
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