ArticleAntioxidants & redox signaling2014
Reactive oxygen species deficiency induces autoimmunity with type 1 interferon signature.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 133 citations in OpenAlex.
- Systemic lupus erythematosus with lupus nephritis in a child with chronic granulomatous disease: a diagnostic and therapeutic challenge.Pediatric nephrology (Berlin, Germany) · 2026Article
- NADPH oxidase 2 (NOX2)-independent inducers of neutrophil extracellular traps promote resolution of chronic inflammation.Redox biology · 2026Article
- Dysregulation of U12-Type Splicing in Lupus Neutrophils.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Neutrophils as critical orchestrators of chronic inflammation.Cellular & molecular immunology · 2026Review
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- Dysregulation of U12-Type Splicing in Lupus Neutrophils.bioRxiv : the preprint server for biology · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- The Role of NADPH Oxidase 2 in Leukocytes.Antioxidants (Basel, Switzerland) · 2025Review
- The systemic lupus erythematosus-associated NCF1Nature communications · 2025Article
- Spontaneous NETosis and type I IFN signaling activation in resting neutrophils of chronic granulomatous disease patients withGenes & diseases · 2024Article
- Multifaceted Proteome Analysis at Solubility, Redox, and Expression Dimensions for Target Identification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mechanism and target treatment of primary immunodeficiency diseases with systemic lupus erythematosus-like phenotype.Pediatric discovery · 2024Review
- Ncf1 knockout in smooth muscle cells exacerbates angiotensin II-induced aortic aneurysm and dissection by activating the STING pathway.Cardiovascular research · 2024Article
- NADPH oxidase in B cells and macrophages protects against murine lupus by regulation of TLR7.JCI insight · 2024Article
- Exploring the ROS reduction strategies in chronic lupus management.Frontiers in immunology · 2024Article
- Clinical presentation, diagnosis, and treatment of chronic granulomatous disease.Frontiers in pediatrics · 2024Review
- Peripheral T Cell Populations are Differentially Affected in Familial Mediterranean Fever, Chronic Granulomatous Disease, and Gout.Journal of clinical immunology · 2023Article
- The association of APOH and NCF1 polymorphisms on susceptibility to recurrent pregnancy loss in women with antiphospholipid syndrome.Journal of assisted reproduction and genetics · 2023Article
- NCF1-dependent production of ROS protects against lupus by regulating plasmacytoid dendritic cell development and functions.JCI insight · 2023Article
- The paradox of autoimmunity and autoinflammation in inherited neutrophil disorders - in search of common patterns.Frontiers in immunology · 2023Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 10 institutions in 4 countries.
Funding
Abstract
aimsChronic granulomatous disease (CGD) is a primary immunodeficiency caused by mutations in the phagocyte reactive oxygen species (ROS)-producing NOX2 enzyme complex and characterized by recurrent infections associated with hyperinflammatory and autoimmune manifestations. A translational, comparative analysis of CGD patients and the corresponding ROS-deficient Ncf1(m1J) mutated mouse model was performed to reveal the molecular pathways operating in NOX2 complex deficient inflammation.
resultsA prominent type I interferon (IFN) response signature that was accompanied by elevated autoantibody levels was identified in both mice and humans lacking functional NOX2 complex. To further underline the systemic lupus erythematosus (SLE)-related autoimmune process, we show that naïve Ncf1(m1J) mutated mice, similar to SLE patients, suffer from inflammatory kidney disease with IgG and C3 deposits in the glomeruli. Expression analysis of germ-free Ncf1(m1J) mutated mice reproduced the type I IFN signature, enabling us to conclude that the upregulated signaling pathway is of endogenous origin. INNOVATION: Our findings link the previously unexplained connection between ROS deficiency and increased susceptibility to autoimmunity by the discovery that activation of IFN signaling is a major pathway downstream of a deficient NOX2 complex in both mice and humans.
conclusionWe conclude that the lack of phagocyte-derived oxidative burst is associated with spontaneous autoimmunity and linked with type I IFN signature in both mice and humans.
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