Medical Journals

B Cell Receptor Cross-talk: Exposure to Lipopolysaccharide Induces an Alternate Pathway for B Cell Receptor-induced Erk Phosphorylation and Nf-kappa B Activation.

Authors:
  • Dye John R
  • Palvanov Arkadiy
  • Guo Benchang
  • Rothstein Thomas L

From: Department of Pathology, Boston University School of Medicine, Boston, MA 02118, USA.

Journal of immunology (Baltimore, Md. : 1950)

  • Publish Date: Jul 2007
  • ISSN: 0022-1767
  • Volume: 179
  • Issue: 1
  • Pages: 229-35
  • Medium: Print
  • Language: English
  • Citation (JAMA): Dye John R, Palvanov Arkadiy, Guo Benchang, et al. B Cell Receptor Cross-talk: Exposure to Lipopolysaccharide Induces an Alternate Pathway for B Cell Receptor-induced Erk Phosphorylation and Nf-kappa B Activation.. J. Immunol. Jul 2007;179:229-35

Abstract

BCR signaling in naive B cells depends on the function of signalosome mediators; however, prior engagement of CD40 or of IL-4R produces an alternate signaling pathway in which Bruton’s tyrosine kinase, PI3K, phospholipase Cgamma2, and protein kinase Cbeta are no longer required for BCR-induced downstream events. To explore the range of mediators capable of producing such an alternate pathway for BCR signaling, we examined the TLR4 agonist, LPS. B cell treatment with LPS at relatively low doses altered subsequent BCR signaling such that ERK phosphorylation and NF-kappaB activation occurred in a PI3K-independent manner. This effect of LPS extended to MEK phosphorylation and IkappaBalpha degradation, and it developed slowly over a period of 16-24 h. The involvement of TLRs is suggested by similar effects observed with a structurally distinct TLR agonist, PAM3CSK4 and by the need for MyD88 for induction of alternate BCR signaling by LPS. Thus, LPS-mediated TLR engagement produces an alternate pathway for BCR-triggered signal propagation that differs from the classical, signalosome-dependent pathway.

Mesh Headings (Keywords): 1-Phosphatidylinositol 3-Kinase, Animals, B-Lymphocyte Subsets, Cells, Cultured, Chromones, Enzyme Inhibitors, Extracellular Signal-Regulated MAP Kinases, Lipopolysaccharides, MAP Kinase Kinase 1, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Morpholines, Myeloid Differentiation Factor 88, NF-kappa B, Phosphorylation, Receptor Cross-Talk, Receptors, Antigen, B-Cell, Signal Transduction, Time Factors


Check for Full Text / PubMed Unique Identifier (PMID): 17579042


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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