Linked Life Data

19828630

Source:http://linkedlifedata.com/resource/pubmed/id/19828630

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2009-10-21
pubmed:abstractText
NK cells vigorously proliferate during viral infections, resulting in an expanded pool of innate lymphocytes that are able to participate in early host defense. The relative contributions of cytokines and activation receptors in stimulating NK cell proliferation during viral infections are not well characterized. In this study, we demonstrated that signaling through the NK cell activation receptor Ly49H was able to compensate for the absence of cytokine stimulation in the preferential phase of viral-induced proliferation during murine cytomegalovirus infection. In the absence of type I IFN stimulation, NK cell proliferation was strongly biased toward cells expressing the Ly49H receptor, even at early time points when minimal preferential Ly49H-mediated proliferation was observed in wild-type mice. In the absence of effective Ly49H signaling or following infection with virus that did not express the ligand for Ly49H, no difference was observed in the proliferation of subsets of NK cells that either express or lack expression of Ly49H, although the overall proliferation of NK cells in IFNalphabetaR(-/-) mice was substantially reduced. These results highlight the contribution of NK cell activation receptors in stimulating proliferation and subsequent expansion of NK cells that are able to recognize virally infected cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
183
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5830-6
pubmed:dateRevised
2011-5-5
pubmed:meshHeading
pubmed-meshheading:19828630-Adaptor Proteins, Signal Transducing, pubmed-meshheading:19828630-Animals, pubmed-meshheading:19828630-Cell Proliferation, pubmed-meshheading:19828630-Gene Knock-In Techniques, pubmed-meshheading:19828630-Herpesviridae Infections, pubmed-meshheading:19828630-Killer Cells, Natural, pubmed-meshheading:19828630-Lymphocyte Activation, pubmed-meshheading:19828630-Mice, pubmed-meshheading:19828630-Mice, Inbred BALB C, pubmed-meshheading:19828630-Mice, Inbred C57BL, pubmed-meshheading:19828630-Mice, Knockout, pubmed-meshheading:19828630-Muromegalovirus, pubmed-meshheading:19828630-NIH 3T3 Cells, pubmed-meshheading:19828630-NK Cell Lectin-Like Receptor Subfamily A, pubmed-meshheading:19828630-Receptor, Interferon alpha-beta, pubmed-meshheading:19828630-Signal Transduction
pubmed:year
2009
pubmed:articleTitle
Ly49H engagement compensates for the absence of type I interferon signaling in stimulating NK cell proliferation during murine cytomegalovirus infection.
pubmed:affiliation
Division of Pediatric Rheumatology, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural