The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/7/93/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 1, July 1, 1998 93-101

Articles

The Molecular Mechanism of B Cell Activation by toll-like Receptor Protein RP-105

Vivien W.F. Chan*, Ingrid Mecklenbräuker{ddagger},§, I-hsin Su{ddagger},§, Gemma Texido§, Michael Leitges||, Rita Carsetti||, Clifford A. Lowell*, Klaus Rajewsky§, Kensuke Miyake, and Alexander Tarakhovsky{ddagger},§

From the * Department of Laboratory Medicine, University of California, San Francisco, California 94143; {ddagger} Laboratory of Lymphocyte Signaling and § Department of Immunology, Institute for Genetics, University of Köln, Weyertal 121, D-50931 Köln, Germany; || Max-Planck-Institut für Immunbiologie, Stubeweg 51, D-79108 Freiburg, Germany; and Department of Immunology, Saga Medical School, Nabeshima, Saga 849, Japan

The B cell–specific transmembrane protein RP-105 belongs to the family of Drosophila toll-like proteins which are likely to trigger innate immune responses in mice and man. Here we demonstrate that the Src-family protein tyrosine kinase Lyn, protein kinase C β I/II (PKCβI/II), and Erk2-specific mitogen-activated protein (MAP) kinase kinase (MEK) are essential and probably functionally connected elements of the RP-105–mediated signaling cascade in B cells. We also find that negative regulation of RP-105–mediated activation of MAP kinases by membrane immunoglobulin may account for the phenomenon of antigen receptor–mediated arrest of RP-105–mediated B cell proliferation.

Key Words: RP-105 • B lymphocytes • signal transduction • mice

Address correspondence to Alexander Tarakhovsky, Laboratory of Lymphocyte Signaling, Institute for Genetics, University of Köln, Weyertal 121, D-50931 Köln, Germany. Phone: 49-221-470 4319; Fax: 49-221-470 4970; E-mail: sasha{at}mac.genetik.uni-koeln.de

Abbreviations used: BCR, B cell antigen receptor; CsA, cyclosporin A; dnMEK, double negative mutant of MEK; Fc{gamma}R, Fc{gamma} receptors; MAP, mitogen-activated protein; MEK, MAP kinase kinase; PAMPS, pathogen-associated molecular pattern; PKCβI/II, protein kinase C β I/II; PRR, pattern recognition receptor; PTK, protein tyrosine kinase; sIgM, surface IgM.


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