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Blood, 1 September 2007, Vol. 110, No. 5, pp. 1530-1539. Prepublished online as a Blood First Edition Paper on May 10, 2007; DOI 10.1182/blood-2006-10-048173. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-10-048173v1 110/5/1530    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Wang, H. Articles by Verneris, M. R. Search for Related Content PubMed PubMed Citation Articles by Wang, H. Articles by Verneris, M. R. Related Collections Immunobiology Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY The unexpected effect of cyclosporin A on CD56+CD16– and CD56+CD16+ natural killer cell subpopulations Hongbo Wang1, Bartosz Grzywacz1, David Sukovich1, Valarie McCullar2, Qing Cao3, Alisa B. Lee1, Bruce R. Blazar1, David N. Cornfield4, Jeffrey S. Miller2, and Michael R. Verneris1 Departments of1 Pediatrics and 2 Medicine, Division of Blood and Marrow Transplantation; 3 Biostatistics Shared Resource, Cancer Center, University of Minnesota, Minneapolis; 4 Department of Pediatrics, Stanford University School of Medicine, Palo Alto, CA Cyclosporin A (CSA) is commonly used to prevent graft-versus-host disease. The influence of CSA on T-cell function has been extensively investigated; however, the effect of CSA on natural killer (NK) cells is less understood. NK cells were cultured with IL-2 and IL-15 with and without CSA for 1 week. Compared with controls, CSA-treated cultures showed fewer CD56+CD16+KIR+ NK cells and a reciprocal increase in CD56+CD16–KIR– cells. These changes were due mainly to a reduced proliferation of the CD56dim NK-cell subpopulation and a relative resistance of CD56bright NK cells to CSA. Following coculture with K562 targets, CSA-exposed NK cells differed from controls and lacked Ca2+ oscillations, nuclear factor of activated T cells (NFAT) dephosphorylation, and NFAT nuclear translocation. NK cells cultured in CSA retained cytotoxicity against K562, Raji, and KIR ligand-expressing lymphoblastoid cells. NK cells cultured in CSA showed increases in NKp30 and reductions in NKp44 and NKG2D. Following IL-12 and IL-18 stimulation, CSA-treated NK cells showed more IFN-–producing cells. Using in vitro NK-cell differentiation, progenitor cells gave rise to more CD56+KIR– NK cells in the presence of CSA than controls. Collectively, these studies show that CSA influences NK-cell function and phenotype, which may have important implications for graft-versus-leukemia effects. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. G. Brunstein, J. E. Wagner, D. J. Weisdorf, S. Cooley, H. Noreen, J. N. Barker, T. DeFor, M. R. Verneris, B. R. Blazar, and J. S. Miller Negative effect of KIR alloreactivity in recipients of umbilical cord blood transplant depends on transplantation conditioning intensity Blood, May 28, 2009; 113(22): 5628 - 5634. [Abstract] [Full Text] [PDF] G. Weitz-Schmidt, S. Chreng, and S. Riek Allosteric LFA-1 Inhibitors Modulate Natural Killer Cell Function Mol. Pharmacol., February 1, 2009; 75(2): 355 - 362. [Abstract] [Full Text] [PDF] E. M. Dunbar, M. P. Buzzeo, J. B. Levine, J. D. Schold, H.-U. Meier-Kriesche, and V. Reddy The relationship between circulating natural killer cells after reduced intensity conditioning hematopoietic stem cell transplantation and relapse-free survival and graft-versus-host disease Haematologica, December 1, 2008; 93(12): 1852 - 1858. [Abstract] [Full Text] [PDF] C. Sabella, E. Faszewski, L. Himic, K. M. Colpitts, J. Kaltenbach, M. M. Burger, and X. Fernandez-Busquets Cyclosporin A Suspends Transplantation Reactions in the Marine Sponge Microciona prolifera J. Immunol., November 1, 2007; 179(9): 5927 - 5935. [Abstract] [Full Text] [PDF]

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