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Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 December 2001, Vol. 98, No. 13, pp. 3554-3561 CHEMOKINES Amino-terminal truncation of CXCR3 agonists impairs receptor signaling and lymphocyte chemotaxis, while preserving antiangiogenic properties Paul Proost, Evemie Schutyser, Patricia Menten, Sofie Struyf, Anja Wuyts, Ghislain Opdenakker, Michel Detheux, Marc Parmentier, Christine Durinx, Anne-Marie Lambeir, Johan Neyts, Sandra Liekens, Prabhat C. Maudgal, Alfons Billiau, and Jo Van Damme From the Laboratories of Molecular Immunology, Experimental Chemotherapy, and Immunobiology, Rega Institute for Medical Research, and Department of Ophthalmology, Catholic University of Leuven, Belgium; IRIBHN and Euroscreen SA, Université Libre de Bruxelles, Belgium; and Laboratory of Clinical Biochemistry, University of Antwerp, Wilrijk, Belgium. The interferon (IFN)-inducible chemokines, specifically, IFN--inducible protein-10 (IP-10), monokine induced by IFN- (Mig), and IFN-inducible T-cell -chemoattractant (I-TAC), share a unique CXC chemokine receptor (CXCR3). Recently, the highly specific membrane-bound protease and lymphocyte surface marker CD26/dipeptidyl peptidase IV (DPP IV) was found to be responsible for posttranslational processing of chemokines. Removal of NH2-terminal dipeptides by CD26/DPP IV alters chemokine receptor binding and signaling, and hence inflammatory and anti-human immunodeficiency virus (HIV) activities. CD26/DPP IV and CXCR3 are both markers for Th1 lymphocytes and, moreover, CD26/DPP IV is present in a soluble, active form in human plasma. This study reports that at physiologic enzyme concentrations CD26/DPP IV cleaved 50% of I-TAC within 2 minutes, whereas for IP-10 and Mig the kinetics were 3- and 10-fold slower, respectively. Processing of IP-10 and I-TAC by CD26/DPP IV resulted in reduced CXCR3-binding properties, loss of calcium-signaling capacity through CXCR3, and more than 10-fold reduced chemotactic potency. Moreover, IP-10 and I-TAC cleaved by CD26/DPP IV acted as chemotaxis antagonists and CD26/DPP IV-truncated IP-10 and Mig retained their ability to inhibit the angiogenic activity of interleukin-8 in the rabbit cornea micropocket model. These data demonstrate a negative feedback regulation by CD26/DPP IV in CXCR3-mediated chemotaxis without affecting the angiostatic potential of the CXCR3 ligands IP-10 and Mig. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: X.-Y. Du and L. L.K. Leung Proteolytic regulatory mechanism of chemerin bioactivity Acta Biochim Biophys Sin, November 12, 2009; (2009) gmp091v1. [Abstract] [Full Text] [PDF] Z. Liu, M. Christensson, A. Forslow, I. De Meester, and K.-G. Sundqvist A CD26-Controlled Cell Surface Cascade for Regulation of T Cell Motility and Chemokine Signals J. Immunol., September 15, 2009; 183(6): 3616 - 3624. [Abstract] [Full Text] [PDF] T. Loos, A. Mortier, M. Gouwy, I. Ronsse, W. Put, J.-P. Lenaerts, J. Van Damme, and P. 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