Sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis

Yuhsuke Ohmi, Wataru Ise, Akira Harazono, Daisuke Takakura, Hidehiro Fukuyama, Yoshihiro Baba, Masashi Narazaki, Hirofumi Shoda, Nobunori Takahashi, Yuki Ohkawa, Shuting Ji, Fumihiro Sugiyama, Keishi Fujio, Atsushi Kumanogoh, Kazuhiko Yamamoto, Nana Kawasaki, Tomohiro Kurosaki, Yoshimasa Takahashi () and Koichi Furukawa ()
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Yuhsuke Ohmi: Nagoya University Graduate School of Medicine
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
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
Tomohiro Kurosaki: Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center and Graduate School of Frontier Biosciences, Osaka University
Yoshimasa Takahashi: National Institute of Infectious Diseases
Koichi Furukawa: Nagoya University Graduate School of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms11205

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