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

Shin-ichiro Honda, Kazuki Sato, Naoya Totsuka, Satoshi Fujiyama, Manabu Fujimoto, Kensuke Miyake, Chigusa Nakahashi-Oda, Satoko Tahara-Hanaoka, Kazuko Shibuya and Akira Shibuya ()
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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
Kazuko Shibuya: Faculty of Medicine, University of Tsukuba
Akira Shibuya: Faculty of Medicine, University of Tsukuba

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms11498

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