|
|
A failure to degrade DNA properly may contribute to the development of rheumatoid arthritis, a mouse study suggests.
Every day in the human body, hundreds of millions of cells commit suicide, expelling their DNA along the way. This, and other excess DNA, is engulfed by scavenger cells called macrophages, which break it down using an enzyme called DNase II. But mice lacking the enzyme develop rheumatoid-arthritis-like symptoms, Shigekazu Nagata and colleagues report in a paper published in the 26 October 2006 issue of Nature (Vol. 443, No. 7114, pp 998-1002). Macrophages without DNase II, carrying the undigested DNA, produce the inflammatory tumour necrosis factor (TNF-alpha) protein, and treatment with an anti-TNF-alpha antibody prevents the mice from developing symptoms. CONTACT Shigekazu Nagata (Osaka University Medical School, Japan) E-mail: nagata@genetic.med.osaka-u.ac.jp (C) Nature press release.
Message posted by: Trevor M. D'Souza
|
|
Variants Associated with Pediatric Allergic Disorder
Mutations in PHF6 Found in T-Cell Leukemia
Genetic Risk Variant for Urinary Bladder Cancer
Antibody Has Therapeutic Effect on Mice with ALS
Regulating P53 Activity in Cancer Cells
Anti-RNA Therapy Counters Breast Cancer Spread
Mitochondrial DNA Diversity
The Power of RNA Sequencing
‘Pro-Ageing' Therapy for Cancer?
Niche Genetics Influence Leukaemia
Molecular Biology: Clinical Promise for RNA Interference
Chemoprevention Cocktail for Colon Cancer
more news ...
|