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      Leukocyte-Endothelial Cell Interactions – Lessons from Knockout Mice

      ,

      Cardiorenal Medicine

      S. Karger AG

      Knockout mice, Inflammation, Adhesion receptors, Glomerulonephritis

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          Abstract

          The advent of gene targeting has led to the generation of several mouse strains deficient in select leukocyte adhesion receptors. These strains of mice have been very informative about the roles of cell adhesion molecules in leukocyte-endothelium interaction and have produced some surprises: roles for leukocyte adhesion receptors have been demonstrated in development as well as pathologies like obesity, and evidence for functional synergies between adhesion receptors have been provided. We attempt in this review to first outline the technique of gene targeting and give an overview of leukocyte adhesion receptors and mice deficient in these receptors. Second, we discuss models of experimental glomerulonephritis and what we have learned about leukocyte adhesion receptors in the pathogenesis of glomerulonephritis through studies in knockout mice.

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          Most cited references 21

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          Disruption of the proto-oncogene int-2 in mouse embryo-derived stem cells: a general strategy for targeting mutations to non-selectable genes.

          Gene targeting--homologous recombination of DNA sequences residing in the chromosome with newly introduced DNA sequences--in mouse embryo-derived stem cells promises to provide a means to generate mice of any desired genotype. We describe a positive nd negative selection procedure that enriches 2,000-fold for those cells that contain a targeted mutation. The procedure was applied to the isolation of hprt- and int-2- mutants, but it should be applicable to any gene.
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            Lymphocyte homing and leukocyte rolling and migration are impaired in L-selectin-deficient mice.

            L-selectin, a cell adhesion molecule expressed by leukocytes, mediates the attachment of lymphocytes to high endothelial venules (HEV) of peripheral lymph nodes and mediates the earliest interactions between leukocytes and activated vascular endothelium. Mice possessing a mutant L-selectin gene that results in the complete loss of cell surface receptor expression were generated by gene targeting. Lymphocytes from these mice did not bind to peripheral lymph node HEV and these mice had a severe reduction in the number of lymphocytes localized to peripheral lymph nodes. Short-term homing experiments demonstrated that L-selectin was also involved in lymphocyte migration to mucosal lymph nodes, Peyer's patches, and spleen. Furthermore, significant defects in leukocyte rolling and neutrophil migration into the peritoneum in response to an inflammatory stimulus were observed. Thus, L-selectin plays an essential role in leukocyte homing to lymphoid tissues and sites of inflammation.
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              Spontaneous murine lupus-like syndromes. Clinical and immunopathological manifestations in several strains

              MRL/1 and BXSB male mice have a systemic lupus erythematosus (SLE)-like disease similar to but more acute than that occurring in NZB X W mice. The common elements of lymphoid hyperplasia, B-cell hyperactivity, autoantibodies, circulating immune complex (IC), complement consumption, IC glomerulonephritis with gp70 deposition, and thymic atrophy were found in all three kinds of SLE mice. On the basis of these common elements, SLE seen in these mice can be considered a single disease in the same sense that human SLE is one disease. The differences in the SLE expressed in the different mice are no greater than those found in an unselected series of humans with SLE. However, the significant quantitative and qualitative variations in abnormal immunologic expression suggest that different constellations of factors, genetic and/or pathophysiologic, may operate in the three murine strains and that each constellation is capable of leading, via its particular abnormal immunologic consequences, to the activation of common immunopathologic effector mechanisms that cause quite similar SLE-like syndromes. From an experimental point of view, the availability of several inbred murine strains of commonplace histocompatibility types that express an SLE-like syndrome makes possible innumerable manipulations which should help to elucidate the nature and cause(s) of this disorder.
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                Author and article information

                Journal
                EXN
                Nephron Exp Nephrol
                10.1159/issn.1660-2129
                Cardiorenal Medicine
                S. Karger AG
                978-3-8055-6886-9
                978-3-318-00442-7
                1660-2129
                1999
                April 1999
                23 April 1999
                : 7
                : 2
                : 125-136
                Affiliations
                Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass., USA
                Article
                20593 Exp Nephrol 1999;7:125–136
                10.1159/000020593
                10213866
                © 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
                References: 123, Pages: 12
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/20593
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