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Journal of Endotoxin Research
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Essential role of MD-2 in B-cell responses to lipopolysaccharide and Toll-like receptor 4 distribution

Kensuke Miyake

Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan, kmiyake{at}ims.u-tokyo.ac.jp, CREST, Japan Science and Technology Corporation, Tokyo, Japan

Yoshinori Nagai

Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan, CREST, Japan Science and Technology Corporation, Tokyo, Japan

Sachiko Akashi

Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan, CREST, Japan Science and Technology Corporation, Tokyo, Japan

Masakazu Nagafuku

CREST, Japan Science and Technology Corporation, Tokyo, Japan, School of Allied Health Sciences, Faculty of Medicine, Osaka University Medical School, Osaka, Japan

Masato Ogata

Department of Oncogenesis, Osaka University Medical School, Osaka, Japan

Atsushi Kosugi

CREST, Japan Science and Technology Corporation, Tokyo, Japan, School of Allied Health Sciences, Faculty of Medicine, Osaka University Medical School, Osaka, Japan

Toll-like receptor 4 (TLR4) mediates lipopolysaccharide (LPS) signaling in a variety of cell types. MD-2 is associated with the extracellular domain of TLR4 and augments TLR4-dependent LPS responses in vitro. Moreover, mice lacking MD-2 (MD-2— /—) do not respond to LPS, survive endotoxin shock, and are susceptible to Salmonella typhimurium infection. Here, we further show that B cells lacking MD-2 do not up-regulate CD23 in response to LPS. TLR4 predominantly resides in the Golgi apparatus without MD-2. MD-2 is essential for LPS responses in vivo.

Journal of Endotoxin Research, Vol. 8, No. 6, 449-452 (2002)
DOI: 10.1177/09680519020080061401


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