Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation

Leukocyte recruitment from blood to inflammatory sites occurs in a multistep process that involves discrete molecular interactions between circulating and endothelial cells. Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral t...

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Veröffentlicht in:The Journal of immunology (1950) 2005-05, Vol.174 (10), p.6406-6415
Hauptverfasser: Aurrand-Lions, Michel, Lamagna, Chrystelle, Dangerfield, John P, Wang, Shijun, Herrera, Pedro, Nourshargh, Sussan, Imhof, Beat A
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container_end_page 6415
container_issue 10
container_start_page 6406
container_title The Journal of immunology (1950)
container_volume 174
creator Aurrand-Lions, Michel
Lamagna, Chrystelle
Dangerfield, John P
Wang, Shijun
Herrera, Pedro
Nourshargh, Sussan
Imhof, Beat A
description Leukocyte recruitment from blood to inflammatory sites occurs in a multistep process that involves discrete molecular interactions between circulating and endothelial cells. Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral tissues and has been proposed to regulate neutrophil migration by its interaction with the leukocyte integrin Mac-1. In the present study, we show that the accumulation of leukocytes in alveoli during acute pulmonary inflammation in mice is partially blocked using neutralizing Abs against JAM-C. To confirm the function of JAM-C in regulating leukocyte migration in vivo, we then generated a strain of transgenic mice overexpressing JAM-C under the control of the endothelial specific promotor Tie2. The transgenic animals accumulate more leukocytes to inflammatory sites compared with littermate control mice. Intravital microscopy shows that this is the result of increased leukocyte adhesion and transmigration, whereas rolling of leukocytes is not significantly affected in transgenic mice compared with littermates. Thus, JAM-C participates in the later steps of the leukoendothelial adhesion cascade.
doi_str_mv 10.4049/jimmunol.174.10.6406
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Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral tissues and has been proposed to regulate neutrophil migration by its interaction with the leukocyte integrin Mac-1. In the present study, we show that the accumulation of leukocytes in alveoli during acute pulmonary inflammation in mice is partially blocked using neutralizing Abs against JAM-C. To confirm the function of JAM-C in regulating leukocyte migration in vivo, we then generated a strain of transgenic mice overexpressing JAM-C under the control of the endothelial specific promotor Tie2. The transgenic animals accumulate more leukocytes to inflammatory sites compared with littermate control mice. Intravital microscopy shows that this is the result of increased leukocyte adhesion and transmigration, whereas rolling of leukocytes is not significantly affected in transgenic mice compared with littermates. 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subjects Acute Disease
Animals
Cell Adhesion - genetics
Cell Adhesion - immunology
Cell Adhesion Molecules - biosynthesis
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - physiology
Cell Line, Tumor
Chemotaxis, Leukocyte - genetics
Chemotaxis, Leukocyte - immunology
Endothelium - immunology
Endothelium - metabolism
Endothelium - pathology
Granulocytes - cytology
Granulocytes - immunology
Granulocytes - metabolism
Immunoglobulins - biosynthesis
Immunoglobulins - genetics
Immunoglobulins - physiology
Inflammation Mediators - metabolism
Inflammation Mediators - physiology
Lung - immunology
Lung - pathology
Membrane Proteins - biosynthesis
Membrane Proteins - genetics
Membrane Proteins - physiology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Microscopy, Video
Monocytes - cytology
Monocytes - immunology
Monocytes - metabolism
Neutrophil Infiltration - genetics
Neutrophil Infiltration - immunology
Time Factors
title Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation
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