Linked Life Data

11244031

Source:http://linkedlifedata.com/resource/pubmed/id/11244031

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2001-3-13
pubmed:abstractText
This review describes the contribution of noncytolytic mechanisms to the control of viral infections with a particular emphasis on the role of cytokines in these processes. It has long been known that most cell types in the body respond to an incoming viral infection by rapidly secreting antiviral cytokines such as interferon alpha/beta (IFN-alpha/beta). After binding to specific receptors on the surface of infected cells, IFN-alpha/beta has the potential to trigger the activation of multiple noncytolytic intracellular antiviral pathways that can target many steps in the viral life cycle, thereby limiting the amplification and spread of the virus and attenuating the infection. Clearance of established viral infections, however, requires additional functions of the immune response. The accepted dogma is that complete clearance of intracellular viruses by the immune response depends on the destruction of infected cells by the effector cells of the innate and adaptive immune system [natural killer (NK) cells and cytotoxic T cells (CTLs)]. This notion, however, has been recently challenged by experimental evidence showing that much of the antiviral potential of these cells reflects their ability to produce antiviral cytokines such as IFN-gamma and tumor necrosis factor (TNF)-alpha at the site of the infection. Indeed, these cytokines can purge viruses from infected cells noncytopathically as long as the cell is able to activate antiviral mechanisms and the virus is sensitive to them. Importantly, the same cytokines also control viral infections indirectly, by modulating the induction, amplification, recruitment, and effector functions of the immune response and by upregulating antigen processing and display of viral epitopes at the surface of infected cells. In keeping with these concepts, it is not surprising that a number of viruses encode proteins that have the potential to inhibit the antiviral activity of cytokines.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0732-0582
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
65-91
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11244031-Animals, pubmed-meshheading:11244031-Antibodies, Viral, pubmed-meshheading:11244031-Antigen Presentation, pubmed-meshheading:11244031-Antigens, Viral, pubmed-meshheading:11244031-Cytokines, pubmed-meshheading:11244031-Dendritic Cells, pubmed-meshheading:11244031-Granulocytes, pubmed-meshheading:11244031-Humans, pubmed-meshheading:11244031-Immunity, Innate, pubmed-meshheading:11244031-Interferons, pubmed-meshheading:11244031-Killer Cells, Natural, pubmed-meshheading:11244031-Macrophages, pubmed-meshheading:11244031-Mice, pubmed-meshheading:11244031-Mice, Transgenic, pubmed-meshheading:11244031-Models, Immunological, pubmed-meshheading:11244031-T-Lymphocyte Subsets, pubmed-meshheading:11244031-T-Lymphocytes, Helper-Inducer, pubmed-meshheading:11244031-Tumor Necrosis Factor-alpha, pubmed-meshheading:11244031-Viral Proteins, pubmed-meshheading:11244031-Virus Diseases, pubmed-meshheading:11244031-Virus Replication
pubmed:year
2001
pubmed:articleTitle
Noncytolytic control of viral infections by the innate and adaptive immune response.
pubmed:affiliation
Department of Molecular and Experimental Medicine, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA. guidotti@scripps.edu
pubmed:publicationType
Journal Article, Review