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Sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis

Author

Listed:
  • Yuhsuke Ohmi

    (Nagoya University Graduate School of Medicine
    National Institute of Infectious Diseases)

  • Wataru Ise

    (Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center and Graduate School of Frontier Biosciences, Osaka University)

  • Akira Harazono

    (National Institute of Health Sciences)

  • Daisuke Takakura

    (Laboratory of Proteome Science, Graduate School of Medical Life Science, Yokohama City University)

  • Hidehiro Fukuyama

    (Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences)

  • Yoshihiro Baba

    (Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center and Graduate School of Frontier Biosciences, Osaka University)

  • Masashi Narazaki

    (Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine)

  • Hirofumi Shoda

    (Graduate School of Medicine, The University of Tokyo)

  • Nobunori Takahashi

    (Nagoya University Graduate School of Medicine)

  • Yuki Ohkawa

    (Nagoya University Graduate School of Medicine
    Chubu University College of Life and Health Sciences)

  • Shuting Ji

    (Nagoya University Graduate School of Medicine)

  • Fumihiro Sugiyama

    (Laboratory Animal Resource Center, University of Tsukuba)

  • Keishi Fujio

    (Graduate School of Medicine, The University of Tokyo)

  • Atsushi Kumanogoh

    (Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine)

  • Kazuhiko Yamamoto

    (Graduate School of Medicine, The University of Tokyo)

  • Nana Kawasaki

    (National Institute of Health Sciences
    Laboratory of Proteome Science, Graduate School of Medical Life Science, Yokohama City University)

  • Tomohiro Kurosaki

    (Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center and Graduate School of Frontier Biosciences, Osaka University
    Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences)

  • Yoshimasa Takahashi

    (National Institute of Infectious Diseases)

  • Koichi Furukawa

    (Nagoya University Graduate School of Medicine
    Chubu University College of Life and Health Sciences)

Abstract

Rheumatoid arthritis (RA)-associated IgG antibodies such as anti-citrullinated protein antibodies (ACPAs) have diverse glycosylation variants; however, key sugar chains modulating the arthritogenic activity of IgG remain to be clarified. Here, we show that reduced sialylation is a common feature of RA-associated IgG in humans and in mouse models of arthritis. Genetically blocking sialylation in activated B cells results in exacerbation of joint inflammation in a collagen-induced arthritis (CIA) model. On the other hand, artificial sialylation of anti-type II collagen antibodies, including ACPAs, not only attenuates arthritogenic activity, but also suppresses the development of CIA in the antibody-infused mice, whereas sialylation of other IgG does not prevent CIA. Thus, our data demonstrate that sialylation levels control the arthritogenicity of RA-associated IgG, presenting a potential target for antigen-specific immunotherapy.

Suggested Citation

  • Yuhsuke Ohmi & Wataru Ise & Akira Harazono & Daisuke Takakura & Hidehiro Fukuyama & Yoshihiro Baba & Masashi Narazaki & Hirofumi Shoda & Nobunori Takahashi & Yuki Ohkawa & Shuting Ji & Fumihiro Sugiya, 2016. "Sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis," Nature Communications, Nature, vol. 7(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11205
    DOI: 10.1038/ncomms11205
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