Advanced

Ncf1 (p47phox) polymorphism determines oxidative burst and the severity of arthritis in rats and mice.

Hultqvist, Malin LU and Holmdahl, Rikard LU (2005) In Cellular Immunology 233(2). p.97-101
Abstract
Identifying genes that regulate polygenic diseases influenced by the environment such as rheumatoid arthritis (RA), has so far proven to be difficult. By using an alternative approach, i.e., linkage analysis using relevant animal models we succeeded in finding the Ncf1 gene residing in the Pia4 quantitative trait locus to be responsible for the severity of pristane induced arthritis in rats. The influence of another mutation in the mouse Ncf1 gene showed the same association between decreased oxidative burst and enhanced arthritis. In this case the mutation affected a splice site giving a non-detectable oxidative burst response and enhanced collagen induced arthritis as well as myelin oligodendrocyte protein induced experimental autoimmune... (More)
Identifying genes that regulate polygenic diseases influenced by the environment such as rheumatoid arthritis (RA), has so far proven to be difficult. By using an alternative approach, i.e., linkage analysis using relevant animal models we succeeded in finding the Ncf1 gene residing in the Pia4 quantitative trait locus to be responsible for the severity of pristane induced arthritis in rats. The influence of another mutation in the mouse Ncf1 gene showed the same association between decreased oxidative burst and enhanced arthritis. In this case the mutation affected a splice site giving a non-detectable oxidative burst response and enhanced collagen induced arthritis as well as myelin oligodendrocyte protein induced experimental autoimmune encephalomyelitis. These findings open up new possibilities for new treatments for autoimmune diseases, i.e., RA, targeting the NADPH oxidase pathway. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
mice, Ncf1, arthritis, rat, NADPH
in
Cellular Immunology
volume
233
issue
2
pages
97 - 101
publisher
Elsevier
external identifiers
  • wos:000231191100005
  • pmid:15936744
  • scopus:23044447997
ISSN
0008-8749
DOI
10.1016/j.cellimm.2005.04.008
language
English
LU publication?
yes
id
aca8bd92-1ae0-462b-8afc-6536f89dbf62 (old id 140235)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15936744&query_hl=6
date added to LUP
2007-07-30 16:17:03
date last changed
2017-04-09 04:15:51
@article{aca8bd92-1ae0-462b-8afc-6536f89dbf62,
  abstract     = {Identifying genes that regulate polygenic diseases influenced by the environment such as rheumatoid arthritis (RA), has so far proven to be difficult. By using an alternative approach, i.e., linkage analysis using relevant animal models we succeeded in finding the Ncf1 gene residing in the Pia4 quantitative trait locus to be responsible for the severity of pristane induced arthritis in rats. The influence of another mutation in the mouse Ncf1 gene showed the same association between decreased oxidative burst and enhanced arthritis. In this case the mutation affected a splice site giving a non-detectable oxidative burst response and enhanced collagen induced arthritis as well as myelin oligodendrocyte protein induced experimental autoimmune encephalomyelitis. These findings open up new possibilities for new treatments for autoimmune diseases, i.e., RA, targeting the NADPH oxidase pathway.},
  author       = {Hultqvist, Malin and Holmdahl, Rikard},
  issn         = {0008-8749},
  keyword      = {mice,Ncf1,arthritis,rat,NADPH},
  language     = {eng},
  number       = {2},
  pages        = {97--101},
  publisher    = {Elsevier},
  series       = {Cellular Immunology},
  title        = {Ncf1 (p47phox) polymorphism determines oxidative burst and the severity of arthritis in rats and mice.},
  url          = {http://dx.doi.org/10.1016/j.cellimm.2005.04.008},
  volume       = {233},
  year         = {2005},
}