Document Detail


Activation and infection of B cells by Epstein-Barr virus. Role of calcium mobilization and of protein kinase C translocation.
MedLine Citation:
PMID:  2848895     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Both the activation and the transformation of human B cells by EBV were inhibited by either the Ca2+ channel blocking agent verapamil or the combination of theophylline and dibutyryl cAMP: the day 4 and day 20 peaks of [3H]TdR incorporation were abolished; the EBNA marker was not expressed by day 10; lymphoblastoid cell lines did not arise. Short term incubation of B cells with EBV or verapamil showed that the effect of verapamil was reversible and took place early in the interaction between EBV and B cells. The effect of EBV on the early metabolic events of B cell response was thus examined in the presence and in the absence of the drugs. Compared to anti-mu stimulation, supernatant of the transforming B95-8 strain as well as that of the non-transforming P3HR1 strain induced a drug sensitive increase of the free cytosolic Ca2+ concentration. This increase was associated with a protein kinase C translocation from the cytosol to a membrane bound compartment. Moreover, B95-8 supernatant induced phosphatidyl inositol metabolism by human B cells but at least four times less than that induced by anti-mu antibody. These metabolic events induced by EBV were significantly inhibited by anti-CD21 antibodies whereas anti-mu induced metabolic events were not. The infection of EBV negative Ramos cell line was prevented by verapamil or by theophylline + dibutyryl cAMP. Verapamil did not modify the density of EBV receptors but negatively interfered with the penetration of the virus into B cells. Thus B cell activation through the EBV receptor and virus penetration share a common metabolic pathway which is also used for transduction of the signal delivered through the membrane Ig.
Authors:
B Dugas; J F Delfraissy; A Calenda; M Peuchmaur; C Wallon; M T Rannou; P Galanaud
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  141     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  1988 Dec 
Date Detail:
Created Date:  1989-01-18     Completed Date:  1989-01-18     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  4344-51     Citation Subset:  AIM; IM    
Affiliation:
Roussel-Uclaf, Département des Biotechnologies, Romainville, France.
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MeSH Terms
Descriptor/Qualifier:
Antibodies, Anti-Idiotypic
B-Lymphocytes / enzymology,  metabolism*,  ultrastructure
Calcium / metabolism*,  physiology
Cell Line
Cell Membrane / enzymology
Cell Transformation, Viral* / drug effects
Cytosol / enzymology
Herpesvirus 4, Human* / drug effects,  ultrastructure
Humans
Immunoglobulin M / immunology
Inositol Phosphates / biosynthesis
Lymphocyte Activation* / drug effects
Protein Kinase C / metabolism*,  physiology
Verapamil / pharmacology
Chemical
Reg. No./Substance:
0/Antibodies, Anti-Idiotypic; 0/Immunoglobulin M; 0/Inositol Phosphates; 0/anti-IgM; 52-53-9/Verapamil; 7440-70-2/Calcium; EC 2.7.11.13/Protein Kinase C

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


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