Document Detail


Engagement of the CD4 receptor inhibits the interleukin-2-dependent proliferation of human T cells transformed by Herpesvirus saimiri.
MedLine Citation:
PMID:  8149955     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Infection with Herpesvirus saimiri, a tumor virus of non-human primates, transformed human CD4+ T cell clones to permanent interleukin (IL)-2-dependent growth without need for restimulation with antigen and accessory cells. The IL-2-dependent proliferation of these cells was dramatically inhibited by soluble anti-CD4 whole antibodies, F(ab')2 and Fab fragments, and also by gp 120 of human immunodeficiency virus. The inhibition was not due to cell death and could be overcome by high concentrations of exogenous IL-2. Cell surface expression of CD4, and to a lesser degree the density of the IL-2 receptor alpha chain, were reduced upon anti-CD4 treatment. After long lasting (> 12 h) incubation with anti-CD4, abundance and activity of CD4-bound p56lck were diminished while the free fraction of p56lck remained unchanged. Since IL-2 binding to its receptor activated only the CD4-bound fraction of p56lck, the IL-2-induced p56lck activity was diminished after long-term CD4 ligation. Taken together, our results suggest a cross talk between CD4- and IL-2 receptor-mediated signaling via p56lck.
Authors:
B M Bröker; A Y Tsygankov; H Fickenscher; N A Chitaev; I Müller-Fleckenstein; B Fleckenstein; J B Bolen; F Emmrich; H Schulze-Koops
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of immunology     Volume:  24     ISSN:  0014-2980     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  1994 Apr 
Date Detail:
Created Date:  1994-05-09     Completed Date:  1994-05-09     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  843-50     Citation Subset:  IM; X    
Affiliation:
Department of Molecular Biology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton.
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MeSH Terms
Descriptor/Qualifier:
Antibodies, Monoclonal / immunology
Antigens, CD4 / physiology*
Apoptosis
Cell Transformation, Viral*
Cells, Cultured
HIV Envelope Protein gp120 / pharmacology
Herpesvirus 2, Saimiriine / genetics*
Humans
Interleukin-2 / pharmacology*
Lymphocyte Activation*
Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
Proto-Oncogene Proteins / physiology
Receptors, Interleukin-2 / analysis
Signal Transduction
T-Lymphocytes / immunology*
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antigens, CD4; 0/HIV Envelope Protein gp120; 0/Interleukin-2; 0/Proto-Oncogene Proteins; 0/Receptors, Interleukin-2; EC 2.7.10.2/Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
Comments/Corrections
Erratum In:
Eur J Immunol 1994 Jul;24(7):1727

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


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