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

Author

Listed:
  • Kohki Kawane

    (Osaka University Medical School
    Osaka University
    Japan Science and Technology Corporation)

  • Mayumi Ohtani

    (Osaka University Medical School
    Japan Science and Technology Corporation)

  • Keiko Miwa

    (Osaka University Medical School
    Japan Science and Technology Corporation
    RIKEN Kobe Institute)

  • 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
    Osaka University
    Japan Science and Technology Corporation)

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.

Suggested Citation

  • Kohki Kawane & Mayumi Ohtani & Keiko Miwa & Takuji Kizawa & Yoshiyuki Kanbara & Yoshichika Yoshioka & Hideki Yoshikawa & Shigekazu Nagata, 2006. "Chronic polyarthritis caused by mammalian DNA that escapes from degradation in macrophages," Nature, Nature, vol. 443(7114), pages 998-1002, October.
    • Handle: RePEc:nat:nature:v:443:y:2006:i:7114:d:10.1038_nature05245
    DOI: 10.1038/nature05245
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