Linked Life Data

12960267

Source:http://linkedlifedata.com/resource/pubmed/id/12960267

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-10-1
pubmed:abstractText
Deficiency or inhibition of tumor necrosis factor (TNF) significantly prolongs hepatic expression of recombinant adenoviral vectors. To explore mechanisms responsible for this observation, the present studies examined the effects of TNF versus TNF receptor 1 (TNFR1) or TNFR2 deficiency on the course of antiviral-immune responses to a replication-deficient, beta-galactosidase-encoding recombinant adenovirus (AdCMV-lacZ). Clearance of AdCMV-lacZ was significantly delayed in TNF-deficient mice. Less pronounced but significant delays in AdCMV-lacZ clearance were observed in TNFR2-deficient but not TNFR1-deficient mice. Numbers of interferon-gamma expressing intrahepatic lymphocytes (IHL) were similar in AdCMV-lacZ-infected, TNF-deficient, TNFR1-deficient, TNFR2-deficient, and control mice. However, IHL isolated from AdCMV-lacZ-infected, TNF-deficient or AdCMV-lacZ-infected, TNFR2-deficient mice exhibited decreased levels of FasL expression and adenovirus-specific cytolytic T lymphocyte (CTL) activity. Similar defects in allo-specific killing of Fas-sensitive hepatocyte targets by TNF-deficient or TNFR2-deficient but not TNFR1-deficient CTL were also noted. No defects in generation of allo-specific cytotoxicity directed against perforin-sensitive target cells were noted in TNF-, TNFR1-, or TNFR2-deficient lymphocytes. These findings indicate that TNF/TNFR2 interactions facilitate generation of FasL-dependent CTL effector pathways that play an important role in in vivo antiviral-immune responses in the liver.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
564-71
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12960267-Adenoviridae, pubmed-meshheading:12960267-Animals, pubmed-meshheading:12960267-Antigens, CD, pubmed-meshheading:12960267-Cytotoxicity, Immunologic, pubmed-meshheading:12960267-Fas Ligand Protein, pubmed-meshheading:12960267-Interferon-gamma, pubmed-meshheading:12960267-Liver, pubmed-meshheading:12960267-Membrane Glycoproteins, pubmed-meshheading:12960267-Mice, pubmed-meshheading:12960267-Mice, Inbred C3H, pubmed-meshheading:12960267-Mice, Inbred C57BL, pubmed-meshheading:12960267-Mice, Inbred DBA, pubmed-meshheading:12960267-Receptors, Tumor Necrosis Factor, pubmed-meshheading:12960267-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:12960267-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:12960267-T-Lymphocytes, Cytotoxic, pubmed-meshheading:12960267-Tumor Necrosis Factor-alpha
pubmed:year
2003
pubmed:articleTitle
The role of TNF-TNFR2 interactions in generation of CTL responses and clearance of hepatic adenovirus infection.
pubmed:affiliation
Department of Internal Medicine, Divison of Digestive and Liver Diseases, University of Texas Southwestern Medical Center at Dallas, 75390-9151, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.