SEARCH:   Advanced

Blood, 1 October 2004, Vol. 104, No. 7, pp. 2087-2094. Prepublished online as a Blood First Edition Paper on April 29, 2004; DOI 10.1182/blood-2004-02-0696. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-02-0696v1 104/7/2087    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 Bonaparte, M. I. Articles by Barker, E. Search for Related Content PubMed PubMed Citation Articles by Bonaparte, M. I. Articles by Barker, E. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Killing of human immunodeficiency virus-infected primary T-cell blasts by autologous natural killer cells is dependent on the ability of the virus to alter the expression of major histocompatibility complex class I molecules Matthew I. Bonaparte, and Edward Barker From the Department of Microbiology and Immunology, State University of New York, Upstate Medical University, Syracuse, NY. In the current study, we evaluated whether the capacity of HIV to modulate major histocompatibility complex (MHC) class I molecules has an impact on the ability of autologous natural killer (NK) cells to kill the HIV-infected cells. Analysis of HIV-infected T-cell blasts revealed that the decrease in MHC class I molecules on the infected cell surface was selective. HLA-A and -B were decreased on cells infected with HIV strains that could decrease MHC class I molecules, whereas HLA-C and -E remained on the surface. Blocking the interaction between HLA-C and -E and their corresponding inhibitory receptors increased NK cell killing of T-cell blasts infected with HIV strains that reduced MHC class I molecules. Moreover, we demonstrate that NK cells lacking HLA-C and -E inhibitory receptors kill T-cell blasts infected with HIV strains that decrease MHC class I molecules. In contrast, NK cells are incapable of destroying T-cell blasts infected with HIV strains that were unable to reduce MHC class I molecules. These findings suggest that NK cells lacking inhibitory receptors to HLA-C and -E kill HIV-infected CD4+ T cells, and they indicate that the capacity of NK cells to destroy HIV-infected cells depends on the ability of the virus to modulate MHC class I molecules. (Blood. 2004;104:2087-2094) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Iannello, O. Debbeche, S. Samarani, and A. Ahmad Antiviral NK cell responses in HIV infection: II. viral strategies for evasion and lessons for immunotherapy and vaccination J. Leukoc. Biol., July 1, 2008; 84(1): 27 - 49. [Abstract] [Full Text] [PDF] M. R. Schaefer, M. Williams, D. A. Kulpa, P. K. Blakely, A. Q. Yaffee, and K. L. Collins A Novel Trafficking Signal within the HLA-C Cytoplasmic Tail Allows Regulated Expression upon Differentiation of Macrophages J. Immunol., June 15, 2008; 180(12): 7804 - 7817. [Abstract] [Full Text] [PDF] P. Banerjee, G. Feuer, and E. Barker Human T-Cell Leukemia Virus Type 1 (HTLV-1) p12I Down-Modulates ICAM-1 and -2 and Reduces Adherence of Natural Killer Cells, Thereby Protecting HTLV-1-Infected Primary CD4+ T Cells from Autologous Natural Killer Cell-Mediated Cytotoxicity despite the Reduction of Major Histocompatibility Complex Class I Molecules on Infected Cells J. Virol., September 15, 2007; 81(18): 9707 - 9717. [Abstract] [Full Text] [PDF] W. M. Ballan, B.-A. N. Vu, B. R. Long, C. P. Loo, J. Michaelsson, J. D. Barbour, L. L. Lanier, A. A. Wiznia, J. Abadi, G. J. Fennelly, et al. Natural Killer Cells in Perinatally HIV-1-Infected Children Exhibit Less Degranulation Compared to HIV-1-Exposed Uninfected Children and Their Expression of KIR2DL3, NKG2C, and NKp46 Correlates with Disease Severity J. Immunol., September 1, 2007; 179(5): 3362 - 3370. [Abstract] [Full Text] [PDF] C. Tomescu, J. Chehimi, V. C. Maino, and L. J. Montaner NK Cell Lysis of HIV-1-Infected Autologous CD4 Primary T Cells: Requirement for IFN-Mediated NK Activation by Plasmacytoid Dendritic Cells J. Immunol., August 15, 2007; 179(4): 2097 - 2104. [Abstract] [Full Text] [PDF] J. Ward, M. Bonaparte, J. Sacks, J. Guterman, M. Fogli, D. Mavilio, and E. Barker HIV modulates the expression of ligands important in triggering natural killer cell cytotoxic responses on infected primary T-cell blasts Blood, August 15, 2007; 110(4): 1207 - 1214. [Abstract] [Full Text] [PDF] S. Ravet, D. Scott-Algara, E. Bonnet, H. K. Tran, T. Tran, N. Nguyen, L. X. Truong, I. Theodorou, F. Barre-Sinoussi, G. Pancino, et al. Distinctive NK-cell receptor repertoires sustain high-level constitutive NK-cell activation in HIV-exposed uninfected individuals Blood, May 15, 2007; 109(10): 4296 - 4305. [Abstract] [Full Text] [PDF] D. Mavilio, G. Lombardo, J. Benjamin, D. Kim, D. Follman, E. Marcenaro, M. A. O'Shea, A. Kinter, C. Kovacs, A. Moretta, et al. Characterization of CD56-/CD16+ natural killer (NK) cells: A highly dysfunctional NK subset expanded in HIV-infected viremic individuals PNAS, February 22, 2005; 102(8): 2886 - 2891. [Abstract] [Full Text] [PDF]

	Copyright © 2004 by American Society of Hematology         Online ISSN: 1528-0020