Document Detail


B cell receptor (BCR) cross-talk: IL-4 creates an alternate pathway for BCR-induced ERK activation that is phosphatidylinositol 3-kinase independent.
MedLine Citation:
PMID:  15843535     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
IL-4 has pleiotropic effects on B cells. These effects include alteration of subsequent BCR-triggered responses. To identify a molecular basis for this receptor cross-talk, we examined ERK activation and NF-kappaB induction. We found that treatment with IL-4, but not other cytokines, affected subsequent BCR signaling by creating a new pathway in which the need for PI3K in ERK activation was eliminated. In contrast, the need for PI3K in NF-kappaB induction was not altered. The new pathway for ERK required time to develop, depended on STAT6, and was blocked by inhibition of macromolecular synthesis. As in the classical pathway, BCR-induced ERK activation in the new, PI3K-independent pathway required MEK and was reflected in c-Raf. Thus, IL-4 promotes an alternate pathway through which BCR is coupled to Raf/MEK/ERK that may function to heighten the responsiveness of B cells during times of immunological stress.
Authors:
Benchang Guo; Thomas L Rothstein
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  174     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-04-21     Completed Date:  2005-06-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5375-81     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, Boston University School of Medicine, MA 02118, USA.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / physiology*
Animals
B-Lymphocytes / enzymology*,  immunology*,  metabolism
Cells, Cultured
Enzyme Activation / immunology
Extracellular Signal-Regulated MAP Kinases / metabolism*
Interleukin-4 / pharmacology,  physiology*
Male
Mice
Mice, Inbred BALB C
Mice, Knockout
Mice, Transgenic
Mitogen-Activated Protein Kinase 1 / metabolism
NF-kappa B / metabolism
Phosphorylation
Proto-Oncogene Proteins c-raf / metabolism
Receptor Cross-Talk / immunology*
Receptors, Antigen, B-Cell / metabolism*
STAT6 Transcription Factor
Signal Transduction / immunology*
Trans-Activators / deficiency,  genetics,  physiology
Grant Support
ID/Acronym/Agency:
AI40181/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/NF-kappa B; 0/Receptors, Antigen, B-Cell; 0/STAT6 Transcription Factor; 0/Stat6 protein, mouse; 0/Trans-Activators; 207137-56-2/Interleukin-4; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Proto-Oncogene Proteins c-raf; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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