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

doi:10.1084/jem.188.1.93

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J. Exp. Med., Volume 188, Number 1, July 1, 1998 93-101

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

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

From the ^* Department of Laboratory Medicine, University of California, San Francisco, California 94143; 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 totrigger innate immune responses in mice and man. Here we demonstratethat the Src-family protein tyrosine kinase Lyn, protein kinaseC $beta$ I/II (PKC $beta$ I/II), and Erk2-specific mitogen-activated protein(MAP) kinase kinase (MEK) are essential and probably functionallyconnected elements of the RP-105-mediated signaling cascade inB cells. We also find that negative regulation of RP-105-mediatedactivation of MAP kinases by membrane immunoglobulin may accountfor the phenomenon of antigen receptor-mediated arrest of RP-105-mediatedB cell proliferation.

Key words: RP-105; B lymphocytes; signal transduction; mice

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