Positional identification of Ncf1 as a gene that regulates arthritis severity in rats.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/111649
- author
- Olofsson, Peter LU ; Holmberg, Jens LU ; Tordsson, Jesper LU ; Lu, Shemin LU ; Åkerström, Bo LU and Holmdahl, Rikard LU
- organization
- publishing date
- 2003
- 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}}, }