A role for fungal β-glucans and their receptor Dectin-1 in the induction of autoimmune arthritis in genetically susceptible mice

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  • Toshiko Sakihama
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Keiji Hirota
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Satoshi Tanaka
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Takashi Nomura
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Ichiro Miki
    4Department of Allergy, Pharmaceutical Research Center, Kyowa Hakko, Ltd., Shizuoka 411-8731, Japan
  • Siamon Gordon
    6Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
  • Shizuo Akira
    7Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan
  • Takashi Nakamura
    2Department of Orthopedic Surgery, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan
  • Shimon Sakaguchi
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Hiroyuki Yoshitomi
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Katsuya Kobayashi
    4Department of Allergy, Pharmaceutical Research Center, Kyowa Hakko, Ltd., Shizuoka 411-8731, Japan
  • Noriko Sakaguchi
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
  • Gordon D. Brown
    5Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town 7925, South Africa
  • Tomoyuki Tagami
    1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University

書誌事項

公開日
2005-03-21
DOI
  • 10.1084/jem.20041758
公開者
Rockefeller University Press

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説明

<jats:p>A combination of genetic and environmental factors can cause autoimmune disease in animals. SKG mice, which are genetically prone to develop autoimmune arthritis, fail to develop the disease under a microbially clean condition, despite active thymic production of arthritogenic autoimmune T cells and their persistence in the periphery. However, in the clean environment, a single intraperitoneal injection of zymosan, a crude fungal β-glucan, or purified β-glucans such as curdlan and laminarin can trigger severe chronic arthritis in SKG mice, but only transient arthritis in normal mice. Blockade of Dectin-1, a major β-glucan receptor, can prevent SKG arthritis triggered by β-glucans, which strongly activate dendritic cells in vitro in a Dectin-1–dependent but Toll-like receptor-independent manner. Furthermore, antibiotic treatment against fungi can prevent SKG arthritis in an arthritis-prone microbial environment. Multiple injections of polyinosinic-polycytidylic acid double-stranded RNA also elicit mild arthritis in SKG mice. Thus, specific microbes, including fungi and viruses, may evoke autoimmune arthritis such as rheumatoid arthritis by stimulating innate immunity in individuals who harbor potentially arthritogenic autoimmune T cells as a result of genetic anomalies or variations.</jats:p>

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