Chronic polyarthritis caused by mammalian DNA that escapes from degradation in macrophages

Kohki Kawane, Mayumi Ohtani, Keiko Miwa, Takuji Kizawa, Yoshiyuki Kanbara, Yoshichika Yoshioka, Hideki Yoshikawa and Shigekazu Nagata ()
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Kohki Kawane: Osaka University Medical School
Mayumi Ohtani: Osaka University Medical School
Keiko Miwa: Osaka University Medical School
Takuji Kizawa: Osaka University Medical School
Yoshiyuki Kanbara: Iwate Medical University
Yoshichika Yoshioka: Iwate Medical University
Hideki Yoshikawa: Osaka University Medical School
Shigekazu Nagata: Osaka University Medical School

Nature, 2006, vol. 443, issue 7114, 998-1002

Abstract: This year's model The development of drugs for rheumatoid arthritis has not been helped by the lack of a good animal model. Now a newly developed mutant mouse system could help fill the gap. The mice lack the DNaseII gene, and are rescued from the lethal effects of that mutation by a second mutation that permits constitutive production of interferon. They develop chronic polyarthritis, resembling human rheumatoid arthritis, as a result of the failure of DNA degradation during apoptotic cell death and definitive erythropoiesis. This was unexpected: examination of various mouse tissues indicated that macrophages carrying undigested DNA become activated and produce TNF (tumour necrosis factor), leading to the development of polyarthritis. Interestingly TNF is involved in the pathogenesis of rheumatoid arthritis, and anti-TNF treatment is sometimes used to treat the disease.

Date: 2006
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DOI: 10.1038/nature05245

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