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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2205-2213. Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-08-2928. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2928v1 103/6/2205    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 Poggi, A. Articles by Zocchi, M. R. Search for Related Content PubMed PubMed Citation Articles by Poggi, A. Articles by Zocchi, M. R. Related Collections Immunobiology Cell Adhesion and Motility Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Migration of V1 and V2 T cells in response to CXCR3 and CXCR4 ligands in healthy donors and HIV-1–infected patients: competition by HIV-1 Tat Alessandro Poggi, Roberta Carosio, Daniela Fenoglio, Sabrina Brenci, Giuseppe Murdaca, Maurizio Setti, Francesco Indiveri, Silvia Scabini, Elisabetta Ferrero, and Maria Raffaella Zocchi From the Laboratory of Immunology, National Institute for Cancer Research, Genoa, Italy; CEBR and Department of Internal Medicine, DIMI, University of Genoa, Italy; and Laboratory of Tumor Immunology, Scientific Institute San Raffaele, Milan, Italy. We show that HIV-1–infected patients have increased concentrations of circulating V1 T cells (2.2%-9.0% of T lymphocytes; healthy donors, 1.0%-2%) and, in some instances, V2 T cells (3.5%-4.8% vs 2.0%-3.3%). In these patients, both V1 and V2 T cells are CXCR3+CXCR4+, whereas in healthy donors CXCR4 was preferentially expressed on V1 T lymphocytes. T cells transmigrated across endothelial monolayers, in response to interferon-–inducing protein-10 (IP-10/CXCL10), stromal cell–derived factor-1 (SDF-1/CXCL12), or both, according to the expression of the specific receptors CXCR3 and CXCR4. Interestingly, 6Ckine/SLC/CCL21 was more effective than IP-10/CXCL10 on V1 CXCR3+ cells, whereas V2 CXCR3+ cells were driven more efficiently by IP-10/CXCL10. IP-10/CXCL10– and SDF-1/CXCL12–induced transmigration was dependent on phosphoinositide-3 kinase (PI-3K), as demonstrated by the use of the specific blockers wortmannin and LY294002 and by the activation of the downstream serine kinase Akt/PKB on ligation of CXCR3 and CXCR4. Occupancy of CXCR3, but not of CXCR4, led to CAMKII activation; accordingly, the CAMKII inhibitors KN62 and KN93 decreased IP-10/CXCL10– but not SDF-1/CXCL12–driven transmigration. Finally, HIV-1 Tat, which is present in the serum of HIV-1–infected patients, interferes with the chemotactic activity of these chemokines because of the cysteine-rich domain of the protein, which contains CXC and CC chemokine–like sequences. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Fenoglio, A. Poggi, S. Catellani, F. Battaglia, A. Ferrera, M. Setti, G. Murdaca, and M. R. Zocchi V{delta}1 T lymphocytes producing IFN-{gamma} and IL-17 are expanded in HIV-1-infected patients and respond to Candida albicans Blood, June 25, 2009; 113(26): 6611 - 6618. [Abstract] [Full Text] [PDF] E. Faller, J. Kakal, R. Kumar, and P. MacPherson IL-7 and the HIV Tat protein act synergistically to down-regulate CD127 expression on CD8 T cells Int. Immunol., March 1, 2009; 21(3): 203 - 216. [Abstract] [Full Text] [PDF] D. A. Kosub, G. Lehrman, J. M. Milush, D. Zhou, E. Chacko, A. Leone, S. Gordon, G. Silvestri, J. G. Else, P. Keiser, et al. Gamma/Delta T-Cell Functional Responses Differ after Pathogenic Human Immunodeficiency Virus and Nonpathogenic Simian Immunodeficiency Virus Infections J. Virol., February 1, 2008; 82(3): 1155 - 1165. [Abstract] [Full Text] [PDF] J. Kittiworakarn, A. Lecoq, G. Moine, R. Thai, E. Lajeunesse, P. Drevet, C. Vidaud, A. Menez, and M. Leonetti HIV-1 Tat Raises an Adjuvant-free Humoral Immune Response Controlled by Its Core Region and Its Ability to Form Cysteine-mediated Oligomers J. Biol. Chem., February 10, 2006; 281(6): 3105 - 3115. [Abstract] [Full Text] [PDF] M. R. Zocchi, P. Contini, M. Alfano, and A. Poggi Pertussis Toxin (PTX) B Subunit and the Nontoxic PTX Mutant PT9K/129G Inhibit Tat-Induced TGF-{beta} Production by NK Cells and TGF-{beta}-Mediated NK Cell Apoptosis J. Immunol., May 15, 2005; 174(10): 6054 - 6061. [Abstract] [Full Text] [PDF] J. C. Deng, T. A. Moore, M. W. Newstead, X. Zeng, A. M. Krieg, and T. J. Standiford CpG Oligodeoxynucleotides Stimulate Protective Innate Immunity against Pulmonary Klebsiella Infection J. Immunol., October 15, 2004; 173(8): 5148 - 5155. [Abstract] [Full Text] [PDF]

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