ArticleWorld journal of gastroenterology2000
Participation of CD45, NKR-P1A and ANK61 antigen in rat hepatic NK cell (pit cell)mediated target cell cytotoxicity.
Article in World journal of gastroenterology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- The Provocative Roles of Platelets in Liver Disease and Cancer.Frontiers in oncology · 2021Review
- Natural killer cells mediate pathophysiology in response to reduced uterine perfusion pressure.Clinical science (London, England : 1979) · 2017Article
- Expansion and activation of natural killer cells from PBMC for immunotherapy of hepatocellular carcinoma.World journal of gastroenterology · 2004Article
- Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1+ cells.World journal of gastroenterology · 2004Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimSeveral triggering receptors have been described to be involved in natural killer (NK) cell-mediated target cytotoxicity. In these studies, NK cells deriv ed from blood or spleen were used. Pit cells are liver-specific NK cells that possess a higher level of natural cytotoxicity and a different morphology when compared to blood NK cells. The aim of this study was to characterize the role of the NK triggering molecules NKR P1A, ANK61 antigen, and CD45 in pit cell medi ated killing of target cells.
methods( 51) Crrelease and DNA fragmentation were used to quantify target cell lysis and apoptosis, respectively.
resultsFlow cytometric analysis showed that pit cells expressed CD45, NK R P1A, and ANK61 antigen. Treatment of pit cells with monoclonal antibody (mAb)to CD45 (ANK74) not only inhibited CC531s or YAC 1 target lysis but also apopt osis induced by pit cells. The mAbs to NKR P1A (3.2.3) and ANK61 antigen (ANK61 )had no effect on pit cell mediated CC531s or YAC 1 target cytolysis or apopto sis, while they did increase the Fcgamma receptor positive (FcgammaR(+)) P815 cytolysi s and apoptosis. This enhanced cytotoxicity could be inhibited by 3,4 dichloroi socoumarin, an inhibitor of granzymes.
conclusionThese results indicate that CD45 participates in pit cell med iated CC531s and YAC-1 target cytolysis and apoptosis. NKR-P1A and ANK61 antigen on pit cells function as activation structures against Fc gammaR( +) P 815 cells, which was mediated by the perforin/granzyme pathway.
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Registered trials
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