Document Detail


The role of death receptor ligands in shaping tumor microenvironment.
MedLine Citation:
PMID:  17190648     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Death receptor ligands (FasL, TRAIL) activate apoptosis in cells expressing the cognate receptors. Evidence suggests that these ligands also deliver pro-inflammatory signals. In the tumor microenvironment, "Fas counterattack" mounted by tumors against immune cells is mediated by tumor-associated FasL. But death ligands crosslinking their receptors also induce inhibition of apoptosis and activation of the transcription factor, NFkappaB, with a subsequent burst of pro-inflammatory cytokine production and tumor growth promotion. NFkappaB, a key link between inflammation and cancer, regulates dual activities of death ligands, depending on molecular signals in the tumor microenvironment. This paper focuses on death ligands as an example of the extensive repertoire of strategies devised by tumors for escape from immune control.
Authors:
Theresa L Whiteside
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Immunological investigations     Volume:  36     ISSN:  0882-0139     ISO Abbreviation:  Immunol. Invest.     Publication Date:  2007  
Date Detail:
Created Date:  2006-12-27     Completed Date:  2007-03-27     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  8504629     Medline TA:  Immunol Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  25-46     Citation Subset:  IM    
Affiliation:
Department of Pathology, Immunology and Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. whitesidetl@upmc.edu
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MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents / therapeutic use
Fas Ligand Protein / metabolism*
Immunity, Cellular
Inflammation / metabolism
Models, Immunological
Neoplasms / immunology,  metabolism*
Signal Transduction*
TNF-Related Apoptosis-Inducing Ligand / metabolism*
Tumor Escape*
Grant Support
ID/Acronym/Agency:
N0-1 HB37165/HB/NHLBI NIH HHS; P0-1 DE12321/DE/NIDCR NIH HHS; R0-1 CA111786/CA/NCI NIH HHS; R0-1 DE13918/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Fas Ligand Protein; 0/TNF-Related Apoptosis-Inducing Ligand

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


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