The molecular mechanism of B cell activation by toll-like receptor protein RP-105

被引:87
作者
Chan, VWF
Mecklenbräuker, I
Su, IH
Texido, G
Leitges, M
Carsetti, R
Lowell, CA
Rajewsky, K
Miyake, K
Tarakhovsky, A
机构
[1] Univ Koln, Inst Genet, Lab Lymphocyte Signaling, D-50931 Cologne, Germany
[2] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
[3] Univ Koln, Inst Genet, Dept Immunol, D-50931 Cologne, Germany
[4] Max Planck Inst Immunbiol, D-79108 Freiburg, Germany
[5] Saga Med Sch, Dept Immunol, Saga 849, Japan
关键词
RP-105; B lymphocytes; signal transduction; mice;
D O I
10.1084/jem.188.1.93
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 beta I/II (PKC beta I/II), and Erk2-specific mitogen-activated protein (MAP) kinase kiIlase (MEK) are essential and probably functionally connected elements with 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.
引用
收藏
页码:93 / 101
页数:9
相关论文
共 44 条
[1]   INVOLVEMENT OF P59FYN(T) IN INTERLEUKIN-5 RECEPTOR SIGNALING [J].
APPLEBY, MW ;
KERNER, JD ;
CHIEN, S ;
MALISZEWSKI, CR ;
BONDADAA, S ;
PERLMUTTER, RM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (03) :811-820
[2]  
BAIXERAS E, 1993, IMMUNOL REV, V132, P607
[3]   ANTIIMMUNOGLOBULIN STIMULATION OF LYMPHOCYTES-B ACTIVATES SRC-RELATED PROTEIN-TYROSINE KINASES [J].
BURKHARDT, AL ;
BRUNSWICK, M ;
BOLEN, JB ;
MOND, JJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (16) :7410-7414
[4]   MEMBRANE IMMUNOGLOBULIN AND ITS ACCOMPLICES - NEW LESSONS FROM AN OLD RECEPTOR [J].
CAMBIER, JC ;
CAMPBELL, KS .
FASEB JOURNAL, 1992, 6 (13) :3207-3217
[5]   B-cell activation by superstimulatory influenza virus hemagglutinin: A pathogenesis for autoimmunity? [J].
Cash, E ;
Charreire, J ;
Rott, O .
IMMUNOLOGICAL REVIEWS, 1996, 152 :67-88
[6]   Defective negative regulation of antigen receptor signaling in Lyn-deficient B lymphocytes [J].
Chan, VWF ;
Lowell, CA ;
DeFranco, AL .
CURRENT BIOLOGY, 1998, 8 (10) :545-553
[7]   Characterization of the B lymphocyte populations in Lyn-deficient mice and the role of Lyn in signal initiation and down-regulation [J].
Chan, VWF ;
Meng, FY ;
Soriano, P ;
DeFranco, AL ;
Lowell, CA .
IMMUNITY, 1997, 7 (01) :69-81
[8]   INDUCTION OF NF-AT IN NORMAL B-LYMPHOCYTES BY ANTIIMMUNOGLOBULIN OR CD40 LIGAND IN CONJUNCTION WITH IL4 [J].
CHOI, MSK ;
BRINES, RD ;
HOLMAN, MJ ;
KLAUS, GGB .
IMMUNITY, 1994, 1 (03) :179-187
[9]   Signal transduction by the B-cell antigen receptor [J].
DeFranco, AL ;
Richards, JD ;
Blum, JH ;
Stevens, TL ;
Law, DA ;
Chan, VWF ;
Datta, SK ;
Foy, SP ;
Hourihane, SL ;
Gold, MR ;
Matsuuchi, L .
RECEPTOR ACTIVATION BY ANTIGENS, CYTOKINES, HORMONES, AND GROWTH FACTORS, 1995, 766 :195-201
[10]  
FERRERO E, 1990, J IMMUNOL, V145, P331