The Journal of Experimental Medicine
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Published online 26 June 2000.
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© The Rockefeller University Press, 0022-1007/2000/7/23/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 1, July 3, 2000 23-30

Original Article

The Toll-like Receptor Protein RP105 Regulates Lipopolysaccharide Signaling in B Cells

Hirotaka Ogataa, I-hsin Sub, Kensuke Miyakea, Yoshinori Nagaia, Sachiko Akashia, Ingrid Mecklenbräukerb, Klaus Rajewskyc, Masao Kimotoa, and Alexander Tarakhovskyb
a Department of Immunology, Saga Medical School, Saga 849-8501, Japan
b Laboratory of Lymphocyte Signaling, Institute for Genetics, University of Cologne, 50931 Cologne, Germany
c Department of Immunology, Institute for Genetics, University of Cologne, 50931 Cologne, Germany

Correspondence to: Kensuke Miyake, Department of Immunology, Saga Medical School, Nabeshima, Saga 849-8501, Japan. Tel:81-952-34-2256 Fax:81-952-34-2049 E-mail:miyake{at}post.saga-med.ac.jp.

The susceptibility to infections induced by Gram-negative bacteria is largely determined by innate immune responses to bacteria cell wall lipopolysaccharide (LPS). The stimulation of B cells by LPS enhances their antigen-presenting capacity and is accompanied by B cell proliferation and secretion of large quantities of LPS-neutralizing antibodies. Similar to macrophages and neutrophils, the LPS-induced activation of B cells is dependent on Toll-like receptor (TLR)4. Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans. The analysis of mice homozygous for the null mutation in the RP105 gene revealed impaired proliferative and humoral immune responses of RP105-deficient B cells to LPS. Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor {kappa}B activation. These data suggest the existence of the TLR4–RP105 signaling module in the LPS-induced B cell activation.

Key Words: gene targeting, lymphocyte, activation, leucine-rich repeat, cell surface molecule


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