CD43 Interacts With Moesin and Ezrin and Regulates Its Redistribution to the Uropods of T Lymphocytes at the Cell-Cell Contacts
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- Juan M. Serrador
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Marta Nieto
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- José L. Alonso-Lebrero
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Miguel A. del Pozo
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Javier Calvo
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Heinz Furthmayr
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Reinhard Schwartz-Albiez
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Francisco Lozano
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Roberto González-Amaro
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Paloma Sánchez-Mateos
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
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- Francisco Sánchez-Madrid
- From the Servicio de Inmunologı́a, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; the Department of Pathology, Stanford University, Stanford, CA; the School of Medicine, University of San Luis Potosı́, San Luis Potosı́, Mexico; the Servicio de Inmunologı́a, Hospital General Universitario Gregorio Marañón, Madrid, Spain; the Servei d'Immunologia, Hospital Clinic, Barcelona, Spain; and the Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany.
書誌事項
- 公開日
- 1998-06-15
- DOI
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- 10.1182/blood.v91.12.4632
- 公開者
- American Society of Hematology
この論文をさがす
説明
<jats:title>Abstract</jats:title><jats:p>Chemokines as well as the signaling through the adhesion molecules intercellular adhesion molecule (ICAM)-3 and CD43 are able to induce in T lymphocytes their switching from a spherical to a polarized motile morphology, with the formation of a uropod at the rear of the cell. We investigated here the role of CD43 in the regulation of T-cell polarity, CD43-cytoskeletal interactions, and lymphocyte aggregation. Pro-activatory anti-CD43 monoclonal antibody (MoAb) induced polarization of T lymphocytes with redistribution of CD43 to the uropod and the CCR2 chemokine receptor to the leading edge of the cell. Immunofluorescence analysis showed that all three ezrin-radixin-moesin (ERM) actin-binding proteins localized in the uropod of both human T lymphoblasts stimulated with anti-CD43 MoAb and tumor-infiltrating T lymphocytes. Radixin localized at the uropod neck, whereas ezrin and moesin colocalized with CD43 in the uropod. Biochemical analyses showed that ezrin and moesin coimmunoprecipitated with CD43 in T lymphoblasts. Furthermore, in these cells, the CD43-associated moesin increased after stimulation through CD43. The interaction of moesin and ezrin with CD43 was specifically mediated by the cytoplasmic domain of CD43, as shown by precipitation of both ERM proteins with a GST-fusion protein containing the CD43 cytoplasmic tail. Videomicroscopy analysis of homotypic cell aggregation induced through CD43 showed that cellular uropods mediate cell-cell contacts and lymphocyte recruitment. Immunofluorescence microscopy performed in parallel showed that uropods enriched in CD43 and moesin localized at the cell-cell contact areas of cell aggregates. The polarization and homotypic cell aggregation induced through CD43 was prevented by butanedione monoxime, indicating the involvement of myosin cytoskeleton in these phenomena. Altogether, these data indicate that CD43 plays an important regulatory role in remodeling T-cell morphology, likely through its interaction with actin-binding proteins ezrin and moesin. In addition, the redistribution of CD43 to the uropod region of migrating lymphocytes and during the formation of cell aggregates together with the enhancing effect of anti-CD43 antibodies on lymphocyte cell recruitment suggest that CD43 plays a key role in the regulation of cell-cell interactions during lymphocyte traffic.</jats:p>
収録刊行物
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- Blood
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Blood 91 (12), 4632-4644, 1998-06-15
American Society of Hematology