A single nucleotide polymorphism in the NCF1 gene leading to reduced oxidative burst is associated with systemic lupus erythematosus
Objectives Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional N...
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| Published in | Annals of the rheumatic diseases Vol. 76; no. 9; pp. 1607 - 1613 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Limited
01.09.2017
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Objectives Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE).MethodsWe genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes.ResultsWe found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10−20. The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1−6.ConclusionsThese results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. |
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| AbstractList | Objectives: Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE). Methods: We genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes. Results: We found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10-20. The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1-6. Conclusions: These results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. OBJECTIVES: Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE). METHODS: We genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes. RESULTS: We found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10(-20). The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1(-6). CONCLUSIONS: These results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE).OBJECTIVESNcf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE).We genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes.METHODSWe genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes.We found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10-20. The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1-6.RESULTSWe found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10-20. The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1-6.These results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases.CONCLUSIONSThese results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in with systemic lupus erythematosus (SLE). We genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes. We found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10 . The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1 . These results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. Objectives Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE). Methods We genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes. Results We found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0x10(-20) The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0x1(-6). Conclusions These results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. Objectives Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE).MethodsWe genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes.ResultsWe found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10−20. The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1−6.ConclusionsThese results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases. |
| Author | Olsson, Lina M Leonard, Dag Saevarsdottir, Saedis Svenungsson, Elisabet Wetterö, Jonas Bengtsson, Anders A Johansson, Åsa C Gullstrand, Birgitta Jönsen, Andreas Rönnblom, Lars Sjöwall, Christopher Holmdahl, Rikard Gunnarsson, Iva |
| Author_xml | – sequence: 1 givenname: Lina M surname: Olsson fullname: Olsson, Lina M email: rikard.holmdahl@ki.se organization: Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden – sequence: 2 givenname: Åsa C surname: Johansson fullname: Johansson, Åsa C email: rikard.holmdahl@ki.se organization: Division for Hematology and Transfusion Medicine and Division for Clinical Immunology and Transfusion Medicine, Department of Laboratory Medicine, Faculty of Medicine, Lund University, Lund, Sweden – sequence: 3 givenname: Birgitta surname: Gullstrand fullname: Gullstrand, Birgitta email: rikard.holmdahl@ki.se organization: Rheumatology, Department of Clinical Sciences Lund, Faculty of Medicine, Lund University, Lund, Sweden – sequence: 4 givenname: Andreas surname: Jönsen fullname: Jönsen, Andreas email: rikard.holmdahl@ki.se organization: Rheumatology, Department of Clinical Sciences Lund, Faculty of Medicine, Lund University, Lund, Sweden – sequence: 5 givenname: Saedis surname: Saevarsdottir fullname: Saevarsdottir, Saedis email: rikard.holmdahl@ki.se organization: Department of Medicine Solna, Unit of Rheumatology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden – sequence: 6 givenname: Lars surname: Rönnblom fullname: Rönnblom, Lars email: rikard.holmdahl@ki.se organization: Department of Medical Sciences, Science for Life Laboratories, Rheumatology Unit, Uppsala University, Uppsala, Sweden – sequence: 7 givenname: Dag surname: Leonard fullname: Leonard, Dag email: rikard.holmdahl@ki.se organization: Department of Medical Sciences, Science for Life Laboratories, Rheumatology Unit, Uppsala University, Uppsala, Sweden – sequence: 8 givenname: Jonas surname: Wetterö fullname: Wetterö, Jonas email: rikard.holmdahl@ki.se organization: Department of Clinical and Experimental Medicine, Rheumatology/Division of Neuro and Inflammation Sciences, Linköping University, Linköping, Sweden – sequence: 9 givenname: Christopher surname: Sjöwall fullname: Sjöwall, Christopher email: rikard.holmdahl@ki.se organization: Department of Clinical and Experimental Medicine, Rheumatology/Division of Neuro and Inflammation Sciences, Linköping University, Linköping, Sweden – sequence: 10 givenname: Elisabet surname: Svenungsson fullname: Svenungsson, Elisabet email: rikard.holmdahl@ki.se organization: Department of Medicine Solna, Unit of Rheumatology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden – sequence: 11 givenname: Iva surname: Gunnarsson fullname: Gunnarsson, Iva email: rikard.holmdahl@ki.se organization: Department of Medicine Solna, Unit of Rheumatology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden – sequence: 12 givenname: Anders A surname: Bengtsson fullname: Bengtsson, Anders A email: rikard.holmdahl@ki.se organization: Rheumatology, Department of Clinical Sciences Lund, Faculty of Medicine, Lund University, Lund, Sweden – sequence: 13 givenname: Rikard surname: Holmdahl fullname: Holmdahl, Rikard email: rikard.holmdahl@ki.se organization: Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden |
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| ContentType | Journal Article |
| Copyright | Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted. Copyright: 2017 © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted. |
| Copyright_xml | – notice: Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted. – notice: Copyright: 2017 © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted. |
| CorporateAuthor | Avdelningen för hematologi och klinisk immunologi Myeloma research group Rheumatology Institutionen för kliniska vetenskaper, Lund Lunds universitet Profile areas and other strong research environments Department of Laboratory Medicine Lund University Sektion III Reumatologi och molekylär skelettbiologi Institutionen för laboratoriemedicin Myelomgruppen Department of Clinical Sciences, Lund Strategiska forskningsområden (SFO) EpiHealth: Epidemiology for Health Faculty of Medicine Strategic research areas (SRA) Section III Medicinska fakulteten Lund SLE Research Group Profilområden och andra starka forskningsmiljöer Division of Hematology and Clinical Immunology |
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| DOI | 10.1136/annrheumdis-2017-211287 |
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| Keywords | NADPH oxidase complex NCF1 autoimmunity SLE reactive oxygen species |
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NADPH-oxidase complex in autoimmunity publication-title: Arthritis Res Ther doi: 10.1186/ar2299 – volume: 29 start-page: 234 year: 2001 ident: 10.1136/annrheumdis-2017-211287_bib11 article-title: Mutational analysis of patients with p47-phox-deficient chronic granulomatous disease: the significance of recombination events between the p47-phox gene (NCF1) and its highly homologous pseudogenes publication-title: Exp Hematol doi: 10.1016/S0301-472X(00)00646-9 – volume: 73 start-page: 131 year: 2003 ident: 10.1136/annrheumdis-2017-211287_bib10 article-title: Mutational mechanisms of Williams-Beuren syndrome deletions publication-title: Am J Hum Genet doi: 10.1086/376565 – volume: 25 start-page: 1271 year: 1982 ident: 10.1136/annrheumdis-2017-211287_bib15 article-title: The 1982 revised criteria for the classification of systemic lupus erythematosus publication-title: Arthritis Rheum doi: 10.1002/art.1780251101 – volume: 217 start-page: 973 year: 1993 ident: 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disease publication-title: Nat Med doi: 10.1038/nm.4027 – volume: 101 start-page: 12646 year: 2004 ident: 10.1136/annrheumdis-2017-211287_bib2 article-title: Enhanced autoimmunity, arthritis, and encephalomyelitis in mice with a reduced oxidative burst due to a mutation in the Ncf1 gene publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.0403831101 – volume: 148 start-page: 79 year: 2007 ident: 10.1136/annrheumdis-2017-211287_bib5 article-title: Cutaneous and other lupus-like symptoms in carriers of X-linked chronic granulomatous disease: incidence and autoimmune serology publication-title: Clin Exp Immunol doi: 10.1111/j.1365-2249.2007.03321.x – volume: 97 start-page: 305 year: 2001 ident: 10.1136/annrheumdis-2017-211287_bib12 article-title: Autosomal recessive chronic granulomatous disease caused by defects in NCF-1, the gene encoding the phagocyte p47-phox: mutations not arising in the NCF-1 pseudogenes publication-title: Blood doi: 10.1182/blood.V97.1.305 – volume: 20 start-page: 785 year: 1996 ident: 10.1136/annrheumdis-2017-211287_bib19 article-title: Isoluminol-enhanced chemiluminescence: a sensitive method to study the release of superoxide anion from human neutrophils publication-title: Free Radic Biol Med doi: 10.1016/0891-5849(95)02189-2 – volume: 117 start-page: 3020 year: 2007 ident: 10.1136/annrheumdis-2017-211287_bib28 article-title: Macrophages suppress T cell responses and arthritis development in mice by producing reactive oxygen species publication-title: J Clin Invest doi: 10.1172/JCI31935 – volume: 103 start-page: 12831 year: 2006 ident: 10.1136/annrheumdis-2017-211287_bib27 article-title: T cell surface redox levels determine T cell reactivity and arthritis susceptibility publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.0604571103 – volume: 48 start-page: 940 year: 2016 ident: 10.1136/annrheumdis-2017-211287_bib23 article-title: Genome-wide association meta-analysis in chinese and european individuals identifies ten new loci associated with systemic lupus erythematosus publication-title: Nat Genet doi: 10.1038/ng.3603 – volume: 11 start-page: 13 year: 2010 ident: 10.1136/annrheumdis-2017-211287_bib17 article-title: A copy number variation in human NCF1 and its pseudogenes publication-title: BMC Genet doi: 10.1186/1471-2156-11-13 – volume: 78 start-page: 533 year: 2006 ident: 10.1136/annrheumdis-2017-211287_bib34 article-title: Hemizygosity at the NCF1 gene in patients with Williams-Beuren syndrome decreases their risk of hypertension publication-title: Am J Hum Genet doi: 10.1086/501073 – volume: 33 start-page: 25 year: 2003 ident: 10.1136/annrheumdis-2017-211287_bib1 article-title: Positional identification of Ncf1 as a gene that regulates arthritis severity in rats publication-title: Nat Genet doi: 10.1038/ng1058 – volume: 20 start-page: 511 year: 2014 ident: 10.1136/annrheumdis-2017-211287_bib30 article-title: Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines publication-title: Nat Med doi: 10.1038/nm.3547 – volume: 25 start-page: 983 year: 2016 ident: 10.1136/annrheumdis-2017-211287_bib33 article-title: A reduction in intracellular reactive oxygen Species Due to a mutation in NCF4 promotes autoimmune Arthritis in mice publication-title: Antioxid Redox Signal doi: 10.1089/ars.2016.6675 – volume: 16 start-page: 71 year: 2012 ident: 10.1136/annrheumdis-2017-211287_bib8 article-title: Copy number variation of the gene NCF1 is associated with rheumatoid arthritis publication-title: Antioxid Redox Signal doi: 10.1089/ars.2011.4013 – volume: 100 start-page: 1845 year: 2002 ident: 10.1136/annrheumdis-2017-211287_bib13 article-title: Identification of a novel NCF-1 (p47-phox) pseudogene not containing the signature GT deletion: significance for A47 degrees chronic granulomatous disease carrier detection publication-title: Blood doi: 10.1182/blood-2002-03-0861 – volume: 269 start-page: 228 year: 2016 ident: 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publication-title: Nat Genet doi: 10.1038/ng.3434 – volume: 412 start-page: 15 year: 2007 ident: 10.1136/annrheumdis-2017-211287_bib18 article-title: Isolation of human neutrophils from venous blood publication-title: Methods Mol Biol doi: 10.1007/978-1-59745-467-4_2 – volume: 21 start-page: 2231 year: 2014 ident: 10.1136/annrheumdis-2017-211287_bib21 article-title: Reactive oxygen species deficiency induces autoimmunity with type 1 interferon signature publication-title: Antioxid Redox Signal doi: 10.1089/ars.2013.5828 – volume: 60 start-page: 2418 year: 2009 ident: 10.1136/annrheumdis-2017-211287_bib26 article-title: Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells publication-title: Arthritis Rheum doi: 10.1002/art.24686 – volume: 386 start-page: 401 year: 2005 ident: 10.1136/annrheumdis-2017-211287_bib3 article-title: Activation and assembly of the NADPH oxidase: a structural perspective publication-title: Biochem J doi: 10.1042/BJ20041835 – volume: 3 start-page: 675 year: 2001 ident: 10.1136/annrheumdis-2017-211287_bib14 article-title: The PX domains of p47phox and p40phox bind to lipid products of PI(3)K publication-title: Nat Cell Biol doi: 10.1038/35083070 – volume: 126 start-page: 1953 year: 2016 ident: 10.1136/annrheumdis-2017-211287_bib29 article-title: NADPH oxidase deficiency underlies dysfunction of aged CD8+ Tregs publication-title: J Clin Invest doi: 10.1172/JCI84181 – volume: 50 start-page: 982 year: 2011 ident: 10.1136/annrheumdis-2017-211287_bib20 article-title: The use of systemic lupus erythematosus disease activity Index-2000 to define active disease and minimal clinically meaningful change based on data from a large cohort of systemic lupus erythematosus patients publication-title: Rheumatology doi: 10.1093/rheumatology/keq376 – volume: 49 start-page: 433 year: 2017 ident: 10.1136/annrheumdis-2017-211287_bib24 article-title: A missense variant in NCF1 is associated with susceptibility to multiple autoimmune diseases publication-title: Nat Genet doi: 10.1038/ng.3782 |
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| Snippet | Objectives Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The... polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human gene is... Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1... OBJECTIVES: Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models.... Objectives Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The... Objectives: Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models.... |
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| StartPage | 1607 |
| SubjectTerms | Adult Alleles Animal models Autoimmune diseases autoimmunity Case-Control Studies Clinical Medicine Disease Female Gene Expression Gene Expression Regulation Gene polymorphism Genetic Predisposition to Disease Genomes Genotype & phenotype Genotyping Humans Inflammatory diseases Interferon Klinisk medicin Leukocytes (neutrophilic) Lupus Lupus Erythematosus, Systemic - genetics Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - metabolism Lymphocytes Male Medical and Health Sciences Medicin och hälsovetenskap Mutation NADPH oxidase complex NADPH Oxidases - genetics NCF1 Neutrophils Neutrophils - immunology Polymerase chain reaction Polymorphism, Single Nucleotide Reactive oxygen species Reactive Oxygen Species - metabolism Respiratory Burst - genetics Rheumatoid arthritis Rheumatology Single-nucleotide polymorphism SLE Studies Sweden Systemic lupus erythematosus White People - genetics |
| Title | A single nucleotide polymorphism in the NCF1 gene leading to reduced oxidative burst is associated with systemic lupus erythematosus |
| URI | http://ard.bmj.com/content/76/9/1607.full https://www.ncbi.nlm.nih.gov/pubmed/28606963 https://www.proquest.com/docview/1927723131 https://www.proquest.com/docview/1909228577 https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-139139 https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-333949 https://lup.lub.lu.se/record/d4d93f2c-ccd3-4e46-a04e-3ee44793ab5c oai:portal.research.lu.se:publications/d4d93f2c-ccd3-4e46-a04e-3ee44793ab5c http://kipublications.ki.se/Default.aspx?queryparsed=id:136405180 |
| Volume | 76 |
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