Sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis

نویسندگان

  • 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
  • Koichi Furukawa
چکیده

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.

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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2016