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Blood, 15 February 2004, Vol. 103, No. 4, pp. 1218-1221. Prepublished online as a Blood First Edition Paper on October 23, 2003; DOI 10.1182/blood-2003-02-0576. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2003-02-0576v1 103/4/1218    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, J. Articles by Finkel, T. H. Search for Related Content PubMed PubMed Citation Articles by Wang, J. Articles by Finkel, T. H. Related Collections Immunobiology Signal Transduction Brief Reports Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES Brief report CXCR4 engagement is required for HIV-1–induced L-selectin shedding JiangFang Wang, Susanne Marschner, and Terri H. Finkel From the Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, PA; the Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA; and the Department of Immunology, National Jewish Medical and Research Center, Denver, CO. The chemokine receptor, CXCR4, serves as the primary coreceptor for entry of T-cell tropic human immunodeficiency virus (HIV). Binding of either the CXC-chemokine, stromal-derived factor 1 (SDF-1), or a CXCR4 antagonist, AMD3100, to CXCR4 inhibits infection of CD4+ T cells by T-tropic HIV-1, although only SDF-1 triggers T-cell signaling cascades. We have previously demonstrated that ligation of CD4 by T-cell tropic HIV-1 NL4-3 induces metalloproteinase-dependent L-selectin (CD62L) shedding on resting CD4+ T cells. However, the role of CXCR4 in HIV-induced L-selectin shedding is unclear. Here, we show that L-selectin shedding induced by HIV-1 NL4-3 is completely reversed by AMD3100, but not SDF-1, although SDF-1 alone does not induce L-selectin shedding. These results indicate that engagement of both CD4 and CXCR4 is required for HIV-induced shedding of L-selectin on primary resting CD4+ T cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Ji, J. J-Y. Chen, V. L. Braciale, and M. W. Cloyd Apoptosis induced in HIV-1-exposed, resting CD4+ T cells subsequent to signaling through homing receptors is Fas/Fas ligand-mediated J. Leukoc. Biol., January 1, 2007; 81(1): 297 - 305. [Abstract] [Full Text] [PDF] G. Badr, G. Borhis, D. Treton, C. Moog, O. Garraud, and Y. Richard HIV Type 1 Glycoprotein 120 Inhibits Human B Cell Chemotaxis to CXC Chemokine Ligand (CXCL) 12, CC Chemokine Ligand (CCL)20, and CCL21 J. Immunol., July 1, 2005; 175(1): 302 - 310. [Abstract] [Full Text] [PDF] K. Balabanian, J. Harriague, C. Decrion, B. Lagane, S. Shorte, F. Baleux, J.-L. Virelizier, F. Arenzana-Seisdedos, and L. A. Chakrabarti CXCR4-Tropic HIV-1 Envelope Glycoprotein Functions as a Viral Chemokine in Unstimulated Primary CD4+ T Lymphocytes J. Immunol., December 15, 2004; 173(12): 7150 - 7160. [Abstract] [Full Text] [PDF] N. V. Sipsas and P. P. Sfikakis Expanding Role of Circulating Adhesion Molecules in Assessing Prognosis and Treatment Response in Human Immunodeficiency Virus Infection Clin. Vaccine Immunol., November 1, 2004; 11(6): 996 - 1001. [Full Text] [PDF]

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