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Positional identification of Ncf1 as a gene that regulates arthritis severity in rats.

Olofsson, Peter LU ; Holmberg, Jens LU ; Tordsson, Jesper LU ; Lu, Shemin LU ; Åkerström, Bo LU and Holmdahl, Rikard LU (2003) In Nature Genetics 33(1). p.25-32
Abstract
The identification of genes underlying quantitative-trait loci (QTL) for complex diseases, such as rheumatoid arthritis, is a challenging and difficult task for the human genome project. Through positional cloning of the Pia4 QTL in rats, we found that a naturally occurring polymorphism of Ncf1 (encoding neutrophil cytosolic factor 1, a component of the NADPH oxidase complex) regulates arthritis severity. The disease-related allele of Ncf1 has reduced oxidative burst response and promotes activation of arthritogenic T cells. Pharmacological treatment with substances that activate the NADPH oxidase complex is shown to ameliorate arthritis. Hence, Ncf1 is associated with a new autoimmune mechanism leading to severe destructive arthritis,... (More)
The identification of genes underlying quantitative-trait loci (QTL) for complex diseases, such as rheumatoid arthritis, is a challenging and difficult task for the human genome project. Through positional cloning of the Pia4 QTL in rats, we found that a naturally occurring polymorphism of Ncf1 (encoding neutrophil cytosolic factor 1, a component of the NADPH oxidase complex) regulates arthritis severity. The disease-related allele of Ncf1 has reduced oxidative burst response and promotes activation of arthritogenic T cells. Pharmacological treatment with substances that activate the NADPH oxidase complex is shown to ameliorate arthritis. Hence, Ncf1 is associated with a new autoimmune mechanism leading to severe destructive arthritis, notably similar to rheumatoid arthritis in humans. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Genetics
volume
33
issue
1
pages
25 - 32
publisher
Nature Publishing Group
external identifiers
  • wos:000180136100013
  • pmid:12461526
  • scopus:0037224772
ISSN
1546-1718
DOI
10.1038/ng1058
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Division of Infection Medicine (BMC) (013024020), Medical Inflammation Research (013212019)
id
215b7d3a-1283-4c51-bdc2-d03382bb4691 (old id 111649)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12461526&dopt=Abstract
date added to LUP
2016-04-01 15:48:18
date last changed
2022-03-07 01:29:37
@article{215b7d3a-1283-4c51-bdc2-d03382bb4691,
  abstract     = {{The identification of genes underlying quantitative-trait loci (QTL) for complex diseases, such as rheumatoid arthritis, is a challenging and difficult task for the human genome project. Through positional cloning of the Pia4 QTL in rats, we found that a naturally occurring polymorphism of Ncf1 (encoding neutrophil cytosolic factor 1, a component of the NADPH oxidase complex) regulates arthritis severity. The disease-related allele of Ncf1 has reduced oxidative burst response and promotes activation of arthritogenic T cells. Pharmacological treatment with substances that activate the NADPH oxidase complex is shown to ameliorate arthritis. Hence, Ncf1 is associated with a new autoimmune mechanism leading to severe destructive arthritis, notably similar to rheumatoid arthritis in humans.}},
  author       = {{Olofsson, Peter and Holmberg, Jens and Tordsson, Jesper and Lu, Shemin and Åkerström, Bo and Holmdahl, Rikard}},
  issn         = {{1546-1718}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{25--32}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Genetics}},
  title        = {{Positional identification of Ncf1 as a gene that regulates arthritis severity in rats.}},
  url          = {{http://dx.doi.org/10.1038/ng1058}},
  doi          = {{10.1038/ng1058}},
  volume       = {{33}},
  year         = {{2003}},
}