Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-10-17
pubmed:abstractText
Human cytomegalovirus virus (CMV) is a major cause of morbidity and mortality in immunocompromised individuals. Recently, a novel group of cytokines [interleukin (IL)-28A/B and IL-29, also termed interferon (IFN)-lambdas] has been described. Here, we demonstrate that intestinal epithelial cell (IEC) lines as well as murine and human colonic tissue express the IFN-lambda receptor subunits IL-28R and IL-10R2. IL-28A and IL-29 binding to their receptor complex activates ERK-1/2 and stress-activated protein kinase/c-Jun NH2-terminal kinase MAPKs and Akt, resulting in increased IL-8 protein expression. IFN-lambdas also induce phosphorylation of signal transducer and activator of transcription 1 and significantly increase mRNA expression of suppressor of cytokine signaling 3 and the antiviral proteins myxovirus resistance A and 2',5'-oligoadenylate synthetase. These signals result in an up to 83% reduction of cells positive for human CMV immediate-early protein after human CMV infection. In mice, IL-28A mRNA expression is upregulated after infection with murine CMV in vivo. Both IL-28A and IL-29 significantly decrease cell proliferation but have no effect on Fas-induced apoptosis. In conclusion, IECs express functional receptors for IFN-lambdas, which mediate antiviral and antiproliferative signals in IECs, suggesting a potential for therapeutic use in certain viral infections and as (antiproliferative) anticancer therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/2',5'-Oligoadenylate Synthetase, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/IL28A protein, human, http://linkedlifedata.com/resource/pubmed/chemical/IL29 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8, http://linkedlifedata.com/resource/pubmed/chemical/Interleukins, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/OAS1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytokine, http://linkedlifedata.com/resource/pubmed/chemical/interleukin 28alpha receptor, http://linkedlifedata.com/resource/pubmed/chemical/myxovirus resistance proteins
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0193-1857
pubmed:author
pubmed:issnType
Print
pubmed:volume
289
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G960-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16051921-2',5'-Oligoadenylate Synthetase, pubmed-meshheading:16051921-Animals, pubmed-meshheading:16051921-Apoptosis, pubmed-meshheading:16051921-Cell Line, Tumor, pubmed-meshheading:16051921-Cell Proliferation, pubmed-meshheading:16051921-Colon, pubmed-meshheading:16051921-Cytokines, pubmed-meshheading:16051921-Cytomegalovirus Infections, pubmed-meshheading:16051921-Epithelial Cells, pubmed-meshheading:16051921-GTP-Binding Proteins, pubmed-meshheading:16051921-Gene Expression Regulation, pubmed-meshheading:16051921-Humans, pubmed-meshheading:16051921-Interleukin-8, pubmed-meshheading:16051921-Interleukins, pubmed-meshheading:16051921-Intestinal Mucosa, pubmed-meshheading:16051921-Mice, pubmed-meshheading:16051921-Mice, Inbred C57BL, pubmed-meshheading:16051921-Mitogen-Activated Protein Kinases, pubmed-meshheading:16051921-Receptors, Cytokine, pubmed-meshheading:16051921-Signal Transduction
pubmed:year
2005
pubmed:articleTitle
IL-28A and IL-29 mediate antiproliferative and antiviral signals in intestinal epithelial cells and murine CMV infection increases colonic IL-28A expression.
pubmed:affiliation
Department of Medicine II, University-Hospital Munich-Grosshadern, University of Munich, D-81377 Munich, Germany. stephan.brand@med.uni-muenchen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't