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      Chemokines, Renal Disease, and HIV Infection

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          Abstract

          Renal disease is characterized by the influx of leukocytes into the injured tissue. Before leukocytes can exert their effects on renal damage or repair, they have to reach the site of injury. To recruit specific populations of leukocytes during inflammation is the role of a family of cytokines called chemokines. The characterization of this family has emerged within the past years, yet chemokines have already been the subject of thousands of scientific reports and promise to have many clinical applications. There is good evidence that chemokines contribute to leukocyte infiltration in glomeruli and interstitium and that they play a pivotal role in various renal diseases. The fact that there exist so many chemokines suggests the biological need for redundancy to effect recruitment of immune cells. Although they were originally defined as host defense proteins, chemokines clearly have other functions that extend well beyond the regulation of leukocyte migration. The recent suggestion that chemokines may contribute to a slow progression of the human immunodeficiency virus (HIV) infection and the very recent identification of chemokine receptors as docking molecules for HIV infection add another aspect to chemokine research. The speed at which researchers are exploring the HIV-chemokine connection is evident in the large number of publications on this topic as well as the rapid translation of publications into possible therapeutic applications. Delineating a precise role for chemokines in mediating pathologic changes is an area of fruitful investigation.

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          Most cited references 14

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          The chemokine receptor CXCR4 is essential for vascularization of the gastrointestinal tract.

          Vascularization of organs generally occurs by remodelling of the preexisting vascular system during their differentiation and growth to enable them to perform their specific functions during development. The molecules required by early vascular systems, many of which are receptor tyrosine kinases and their ligands, have been defined by analysis of mutant mice. As most of these mice die during early gestation before many of their organs have developed, the molecules responsible for vascularization during organogenesis have not been identified. The cell-surface receptor CXCR4 is a seven-transmembrane-spanning, G-protein-coupled receptor for the CXC chemokine PBSF/SDF-1 (for pre-B-cell growth-stimulating factor/stromal-cell-derived factor), which is responsible for B-cell lymphopoiesis, bone-marrow myelopoiesis and cardiac ventricular septum formation. CXCR4 also functions as a co-receptor for T-cell-line tropic human immunodeficiency virus HIV-1. Here we report that CXCR4 is expressed in developing vascular endothelial cells, and that mice lacking CXCR4 or PBSF/SDF-1 have defective formation of the large vessels supplying the gastrointestinal tract. In addition, mice lacking CXCR4 die in utero and are defective in vascular development, haematopoiesis and cardiogenesis, like mice lacking PBSF/SDF-1, indicating that CXCR4 is a primary physiological receptor for PBSF/SDF-1. We conclude that PBSF/SDF-1 and CXCR4 define a new signalling system for organ vascularization.
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            A new classification for HIV-1.

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              Chemokine receptors: gateways to inflammation and infection.

               V Schall,  B Premack (1996)
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                1999
                1999
                13 January 1999
                : 81
                : 1
                : 5-16
                Affiliations
                Department of Medicine, Division of Nephrology, University of Hamburg, Germany
                Article
                45239 Nephron 1999;81:5–16
                10.1159/000045239
                9884413
                © 1999 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Tables: 1, References: 109, Pages: 12
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/45239
                Categories
                Molecular Biology in Renal Diseases<br>Section Editor: Prof. F.P. Schena, Bari

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