Document Detail


The role of N-linked carbohydrate residues in lymphokine-activated killer cell-mediated cytolysis.
MedLine Citation:
PMID:  7909499     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We evaluated LAK cell cytotoxicity toward a sensitive B cell lymphoma and several resistant EBV-transformed cell lines in order to explore the mechanism by which some cells are preferentially recognized as targets. Cytolysis of the sensitive cells was inhibited by monoclonal antibodies against the surface proteins LFA-1 and ICAM-1; however, surface expression of ICAM-1 was similar on the resistant and sensitive cell lines. Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1. Treatment of the resistant cells with the endoglycosidase N-glycanase also increased LAK cell sensitivity. Tunicamycin treatment caused a decrease in the molecular weight of ICAM-1 from approximately 95,000 to 50,000 Da. Conjugate formation between the LAK cells and the sensitive and resistant target cells was similar before and after deglycosylation. We conclude that carbohydrate modification of ICAM-1 or an alternative glycoprotein confers resistance to LAK cell cytotoxicity in some cell lines.
Authors:
B A Mehta; H R Collard; R S Negrin
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cellular immunology     Volume:  155     ISSN:  0008-8749     ISO Abbreviation:  Cell. Immunol.     Publication Date:  1994 Apr 
Date Detail:
Created Date:  1994-06-02     Completed Date:  1994-06-02     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  1246405     Medline TA:  Cell Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  95-110     Citation Subset:  IM    
Affiliation:
Department of Medicine, Stanford University Medical Center, California 94305.
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MeSH Terms
Descriptor/Qualifier:
Antibodies, Monoclonal
Cell Adhesion Molecules / immunology
Cell Line, Transformed
Cytotoxicity, Immunologic*
Glycoproteins / immunology*
Glycoside Hydrolases / metabolism
Glycosylation
Herpesvirus 4, Human / genetics
Humans
Intercellular Adhesion Molecule-1
Killer Cells, Lymphokine-Activated / immunology*
Lymphocyte Function-Associated Antigen-1 / immunology
Lymphoma, B-Cell / immunology*
Oligosaccharides / immunology*
Protein Processing, Post-Translational
Tumor Cells, Cultured
Tunicamycin / pharmacology
Grant Support
ID/Acronym/Agency:
RR 05353-29/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Cell Adhesion Molecules; 0/Glycoproteins; 0/Lymphocyte Function-Associated Antigen-1; 0/Oligosaccharides; 11089-65-9/Tunicamycin; 126547-89-5/Intercellular Adhesion Molecule-1; EC 3.2.1.-/Glycoside Hydrolases

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


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