Source:http://linkedlifedata.com/resource/pubmed/id/18941248
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2008-10-22
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pubmed:abstractText |
The heptahelical receptor CD97 is a defining member of the EGF-TM7 family of adhesion class receptors. In both humans and mice, CD97 isoforms are expressed with variable numbers of tandemly arranged N-terminal epidermal growth factor-like domains that facilitate interactions with distinct cellular ligands. Results from treatment of mice with mAbs in various disease models have suggested a role for CD97 in leukocyte trafficking. Here, we aimed to thoroughly characterize the expression profile of CD97, and delineate its biological function. To this end, we applied a novel polyclonal Ab, which is the first antiserum suitable for immunohistochemistry, and combined this analysis with the study of Cd97-lacZ knock-in mice. We show that similar to the situation in humans, hematopoietic, epithelial, endothelial, muscle, and fat cells expressed CD97. Despite this broad expression pattern, the Cd97(-/-) mouse that we created had no overt phenotype, except for a mild granulocytosis. Furthermore, granulocyte accumulation at sites of inflammation was normal in the absence of CD97. Interestingly, application of CD97 mAbs blocked granulocyte trafficking after thioglycollate-induced peritonitis in wild-type but not in knock-out mice. Hence, we conclude that CD97 mAbs actively induce an inhibitory effect that disturbs normal granulocyte trafficking, which is not perturbed by the absence of the molecule.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1550-6606
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pubmed:author |
pubmed-author:AustGabrielaG,
pubmed-author:BeckerSusannS,
pubmed-author:HaaseHanneloreH,
pubmed-author:HamannJörgJ,
pubmed-author:HoekRobert MRM,
pubmed-author:OwensBronwynB,
pubmed-author:VeningaHenrikeH,
pubmed-author:VerbeekJ SjefJS,
pubmed-author:WandelElkeE,
pubmed-author:WobusManjaM,
pubmed-author:de VosAlex FAF,
pubmed-author:van LierRené A WRA,
pubmed-author:van der KaaJosJ,
pubmed-author:van der PollTomT,
pubmed-author:van der ValkMartinM
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
181
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6574-83
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pubmed:meshHeading |
pubmed-meshheading:18941248-Animals,
pubmed-meshheading:18941248-Antibodies,
pubmed-meshheading:18941248-Cell Migration Inhibition,
pubmed-meshheading:18941248-Female,
pubmed-meshheading:18941248-Gene Expression Regulation,
pubmed-meshheading:18941248-Gene Targeting,
pubmed-meshheading:18941248-Granulocytes,
pubmed-meshheading:18941248-Immunophenotyping,
pubmed-meshheading:18941248-Inflammation Mediators,
pubmed-meshheading:18941248-Leukocytosis,
pubmed-meshheading:18941248-Lung,
pubmed-meshheading:18941248-Male,
pubmed-meshheading:18941248-Membrane Glycoproteins,
pubmed-meshheading:18941248-Mice,
pubmed-meshheading:18941248-Mice, Inbred C57BL,
pubmed-meshheading:18941248-Mice, Knockout,
pubmed-meshheading:18941248-Mice, Mutant Strains,
pubmed-meshheading:18941248-Mice, Transgenic,
pubmed-meshheading:18941248-Organ Specificity,
pubmed-meshheading:18941248-Spleen
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pubmed:year |
2008
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pubmed:articleTitle |
Analysis of CD97 expression and manipulation: antibody treatment but not gene targeting curtails granulocyte migration.
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pubmed:affiliation |
Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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