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Marginal zone B cells exacerbate endotoxic shock via interleukin-6 secretion induced by Fcα/μR-coupled TLR4 signalling

Author

Listed:
  • Shin-ichiro Honda

    (Faculty of Medicine, University of Tsukuba)

  • Kazuki Sato

    (Faculty of Medicine, University of Tsukuba)

  • Naoya Totsuka

    (Faculty of Medicine, University of Tsukuba)

  • Satoshi Fujiyama

    (Faculty of Medicine, University of Tsukuba)

  • Manabu Fujimoto

    (Faculty of Medicine, University of Tsukuba)

  • Kensuke Miyake

    (Institute of Medical Sciences, University of Tokyo, Shirokanedai, Minatoloku, Tokyo 108-8639, Japan)

  • Chigusa Nakahashi-Oda

    (Faculty of Medicine, University of Tsukuba)

  • Satoko Tahara-Hanaoka

    (Faculty of Medicine, University of Tsukuba
    Life Science Center of Tsukuba Advanced Research Alliance (TARA), University of Tsukuba)

  • Kazuko Shibuya

    (Faculty of Medicine, University of Tsukuba)

  • Akira Shibuya

    (Faculty of Medicine, University of Tsukuba
    Life Science Center of Tsukuba Advanced Research Alliance (TARA), University of Tsukuba)

Abstract

Marginal zone (MZ) B cells produce a first wave of antibodies for protection from blood-borne pathogens. However, the role of MZ B cells in inflammatory responses has not been elucidated. Here we show that MZ B cells produce pro-inflammatory cytokines, such as interleukin-6 (IL-6), and exacerbate systemic inflammatory responses to lipopolysaccharide (LPS). After intravenous injection of LPS or E. coli, mice deficient in MZ B cells or IL-6 only in MZ B cells have attenuated systemic inflammatory responses and prolonged survival compared with wild-type mice. LPS directly stimulates MZ B cells via Toll-like receptor 4 (TLR4) and MyD88 pathways for IL-6 production. Furthermore, TLR4 requires physical and functional association with Fcα/μR (CD351) for its oligomer formation, NF-κB signalling and IL-6 production from MZ B cells; this association is responsible for systemic inflammatory responses and endotoxic shock. These results reveal a pro-inflammatory role of MZ B cells in endotoxic shock.

Suggested Citation

  • Shin-ichiro Honda & Kazuki Sato & Naoya Totsuka & Satoshi Fujiyama & Manabu Fujimoto & Kensuke Miyake & Chigusa Nakahashi-Oda & Satoko Tahara-Hanaoka & Kazuko Shibuya & Akira Shibuya, 2016. "Marginal zone B cells exacerbate endotoxic shock via interleukin-6 secretion induced by Fcα/μR-coupled TLR4 signalling," Nature Communications, Nature, vol. 7(1), pages 1-10, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11498
    DOI: 10.1038/ncomms11498
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