Luo DZ, Vermijlen D, Ahishali B, Triantis V, Vanderkerken K, Kuppen PJ, Wisse E. Participation of CD45, NKR-P1A and ANK61 antigen in rat hepatic NK cell (pit cell)-mediated target cell cytotoxicity. World J Gastroenterol 2000; 6(4): 546-552 [PMID: 11819644 DOI: 10.3748/wjg.v6.i4.546]
Corresponding Author of This Article
Prof. Dr. Eddie Wisse, Laboratory for Cell Biology and Histology, Free University of Brussels (VUB), Laarbeeklaan 103, B-1090 Brussels, Belgium. wisse@cyto.vub.ac.be
Article-Type of This Article
Original Articles
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Aug 15, 2000; 6(4): 546-552 Published online Aug 15, 2000. doi: 10.3748/wjg.v6.i4.546
Participation of CD45, NKR-P1A and ANK61 antigen in rat hepatic NK cell (pit cell)-mediated target cell cytotoxicity
Dian Zhong Luo, David Vermijlen, Bülent Ahishali, Vasilis Triantis, Karin Vanderkerken, Peter J.K. Kuppen, Eddie Wisse
Dian Zhong Luo, David Vermijlen, Vasilis Triantis, Eddie Wisse, Bü¹lent Ahishali, Laboratory for Cell Biology and Histology.
Karin Vanderkerken, Department of Hematology and Immunology, Free University of Brussels (VUB), Brussels-Jette, Belgium; K Vanderkerken is a postdoctoral researcher of the Fund for Scientific Research Flanders.
Peter J.K. Kuppen, Department of Surgery and Pathology, Leiden University Medical Center, Leiden, The Netherlands
Dian Zhong Luo, Department of Pathology, Guangxi Medical University, Nanning, China
Dian Zhong Luo, Graduated from Guangxi Medical University in 1982, got Master d egrees in 1987 in Guangxi Medical University and in 1994 in Free University of B russels, Professor of Pathology of Guangxi Medical University, and now is following Ph. D. program in Medical Sciences in Free University of Brussels, Belgium, having more than 30 papers published.
Author contributions: All authors contributed equally to the work.
Supported by the grants 3.0053.92, 3.0050.95, 9.0038.96, 1.5.411. 98 from the Nat ional Foundation for Scientific Research (FWO) and the grants 194.322.1740, 195.332.1310, 196.322.0140, and OZR.230 from the Research Council of the Free University of Brussels
Correspondence to: Prof. Dr. Eddie Wisse, Laboratory for Cell Biology and Histology, Free University of Brussels (VUB), Laarbeeklaan 103, B-1090 Brussels, Belgium. wisse@cyto.vub.ac.be
Telephone: +32-2-4774404 Fax: +32-2-4774405
Received: May 22, 2000 Revised: June 10, 2000 Accepted: June 15, 2000 Published online: August 15, 2000
Abstract
AIM: Several triggering receptors have been described to be involved in natural killer (NK) cell-mediated target cytotoxicity. In these studies, NK cells derive d 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 com pared to blood NK cells. The aim of this study was to characterize the role of t he NK-triggeringmoleculesNKR-P1A,ANK61antigen,and CD45 in pit cell-media ted killing of target cells.
METHODS: 51Cr-release and DNA fragmentation were used to quantify target cell lysis and apoptosis, respectively.
RESULTS: Flow 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 apopto sis 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 apoptosis, while they did increase the Fcγ receptor positive (Fcγ R+) P815 cytolysis and apoptosis. This enhanced cytotoxicity could be inhibited by 3,4-dichloroi socoumarin, an inhibitor of granzymes.
CONCLUSION: These results indicate that CD45 participates in pit cell-med iated CC531s and YAC-1 target cytolysis and apoptosis. NKR-P1A and ANK61 antig en on pit cells function as activation structures against Fcγ R+ P 815 cells, which was mediated by the perforin/granzyme pathway.
