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The human OX40/gp34 system directly mediates adhesion of activated T cells to vascular endothelial cells.
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MedLine Citation:
PMID:  8642328     Owner:  NLM     Status:  MEDLINE    
Fresh leukemic cells from patients with adult T cell leukemia (ATL) and some ATL-derived T cell lines show adhesion to human umbilical vein endothelial cells (HUVECs) mainly through E-selectin, but a proportion of this binding remains unaffected by the addition of combinations of antibodies against known adhesion molecules. By immunizing mice with one of such cell lines, we established monoclonal antibodies (mAbs), termed 131 and 315, that recognize a single cell surface antigen (Ag) and inhibit the remaining pathway of the adhesion. These mAbs did not react with normal resting peripheral blood mononuclear cells (PBMC) or most of the cell lines tested except for two other human T cell leukemia virus type I (HTLV-I)-infected T cell lines. After stimulation with phytohemagglutinin (PHA), PBMC expressed Ag 131/315 transiently, indicating that these mAbs define a T cell activation Ag. Western blotting and immunoprecipitation revealed that Ag 131/315 has an apparent molecular mass of 50 kD. Expression cloning was done by transient expression in COS-7 cells and immunological selection to isolate a cDNA clone encoding Ag 131/315. Sequence analysis of the cDNA indicated that it is identical to human OX40, a member of the tumor necrosis factor/nerve growth factor receptor family. We then found that gp34, the ligand of OX40, was expressed on HUVECs and other types of vascular endothelial cells. Furthermore, it was shown that the adhesion of CD4+ cells of PHA-stimulated PBMC to unstimulated HUVECs was considerably inhibited by either 131 or 315. Finally, OX40 transfectants of Kit 225, a human interleukin 2-dependent T cell line, were bound specifically to gp34 transfectants of MMCE, a mouse epithelial cell line, and this binding was blocked by either 315 or 5A8, an anti-gp34 mAb. These results indicate that the OX40/gp34 system directly mediates adhesion of activated T cells or OX40+-transformed T cells to vascular endothelial cells.
A Imura; T Hori; K Imada; T Ishikawa; Y Tanaka; M Maeda; S Imamura; T Uchiyama
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of experimental medicine     Volume:  183     ISSN:  0022-1007     ISO Abbreviation:  J. Exp. Med.     Publication Date:  1996 May 
Date Detail:
Created Date:  1996-07-18     Completed Date:  1996-07-18     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  2985109R     Medline TA:  J Exp Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2185-95     Citation Subset:  IM; X    
Laboratory of AIDS Immunology, Kyoto University, Japan.
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MeSH Terms
Antibodies, Monoclonal
Antigens, CD27 / biosynthesis,  immunology*
Base Sequence
CD4-Positive T-Lymphocytes / immunology,  physiology
Cell Adhesion / immunology
Cell Line
Cells, Cultured
Cercopithecus aethiops
Cloning, Molecular
DNA Primers
Endothelium, Vascular / immunology*
Flow Cytometry
Gene Library
Human T-lymphotropic virus 1 / immunology
Leukemia, T-Cell / immunology*
Mice, Inbred BALB C
Molecular Sequence Data
Polymerase Chain Reaction
Receptors, OX40
Receptors, Tumor Necrosis Factor*
Recombinant Proteins / biosynthesis,  immunology
T-Lymphocytes / physiology*
Tumor Cells, Cultured
Umbilical Veins
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antigens, CD27; 0/DNA Primers; 0/Receptors, OX40; 0/Receptors, Tumor Necrosis Factor; 0/Recombinant Proteins; 0/TNFRSF4 protein, human; 0/Tnfrsf4 protein, mouse

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

Full Text
Journal Information
Journal ID (nlm-ta): J Exp Med
ISSN: 0022-1007
ISSN: 1540-9538
Publisher: The Rockefeller University Press
Article Information
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Print publication date: Day: 1 Month: 5 Year: 1996
Volume: 183 Issue: 5
First Page: 2185 Last Page: 2195
ID: 2192546
Publisher Id: 96235028
PubMed Id: 8642328

The human OX40/gp34 system directly mediates adhesion of activated T cells to vascular endothelial cells

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