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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1997-7-29
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pubmed:abstractText |
Interferons are cytokines that play a complex and central role in the resistance of mammalian hosts to pathogens. Type I interferon (IFN-alpha and IFN-beta) is secreted by virus-infected cells. Immune, type II, or gamma-interferon (IFN-gamma) is secreted by thymus-derived (T) cells under certain conditions of activation and by natural killer (NK) cells. Although originally defined as an agent with direct antiviral activity, the properties of IFN-gamma include regulation of several aspects of the immune response, stimulation of bactericidal activity of phagocytes, stimulation of antigen presentation through class I and class II major histocompatibility complex (MHC) molecules, orchestration of leukocyte-endothelium interactions, effects on cell proliferation and apoptosis, as well as the stimulation and repression of a variety of genes whose functional significance remains obscure. The implementation of such a variety of effects by a single cytokine is achieved by complex patterns of cell-specific gene regulation: Several IFN-gamma-regulated genes are themselves components of transcription factors. The IFN-gamma response is itself regulated by interaction with responses to other cytokines including IFN-alpha/beta, TNF-alpha, and IL-4. Over 200 genes are now known to be regulated by IFN-gamma and they are listed in a World Wide Web document that accompanies this review. However, much of the cellular response to IFN-gamma can be described in terms of a set of integrated molecular programs underlying well-defined physiological systems, for example the induction of efficient antigen processing for MHC-mediated antigen presentation, which play clearly defined roles in pathogen resistance. A promising approach to the complexity of the IFN-gamma response is to extend the analysis of the less understood IFN-gamma-regulated genes in terms of molecular programs functional in pathogen resistance.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antiviral Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Tryptophan,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:issn |
0732-0582
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
749-95
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:9143706-Animals,
pubmed-meshheading:9143706-Antigen Presentation,
pubmed-meshheading:9143706-Antiviral Agents,
pubmed-meshheading:9143706-Apoptosis,
pubmed-meshheading:9143706-Gene Expression Regulation,
pubmed-meshheading:9143706-Humans,
pubmed-meshheading:9143706-Interferon Type I,
pubmed-meshheading:9143706-Interferon-gamma,
pubmed-meshheading:9143706-Models, Biological,
pubmed-meshheading:9143706-Respiratory Burst,
pubmed-meshheading:9143706-Signal Transduction,
pubmed-meshheading:9143706-Tryptophan,
pubmed-meshheading:9143706-Tumor Necrosis Factor-alpha
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pubmed:year |
1997
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pubmed:articleTitle |
Cellular responses to interferon-gamma.
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pubmed:affiliation |
Institute for Genetics, University of Cologne, Köln, Germany. UBOEHM@GENETIK.UNI-KOELN.DE
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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