JAM-C regulates unidirectional monocyte transendothelial migration in inflammation
Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, w...
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| Published in | Blood Vol. 110; no. 7; pp. 2545 - 2555 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Washington, DC
Elsevier Inc
01.10.2007
The Americain Society of Hematology American Society of Hematology |
| Series | Immunobiology |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0006-4971 1528-0020 |
| DOI | 10.1182/blood-2007-03-078733 |
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| Abstract | Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, we show that blockade of JAM-B/-C interaction reduced monocyte numbers in the extravascular compartment through increased reverse transmigration rather than by reduced transmigration. This was confirmed in vivo, showing that an anti–JAM-C antibody reduced the number of monocytes in inflammatory tissue and increased the number of monocytes with a reverse-transmigratory phenotype in the peripheral blood. All together, our results suggest a novel mechanism of reducing accumulation of monocytes at inflammation sites by disruption of JAM-C–mediated monocyte retention. |
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| AbstractList | Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, we show that blockade of JAM-B/-C interaction reduced monocyte numbers in the extravascular compartment through increased reverse transmigration rather than by reduced transmigration. This was confirmed in vivo, showing that an anti–JAM-C antibody reduced the number of monocytes in inflammatory tissue and increased the number of monocytes with a reverse-transmigratory phenotype in the peripheral blood. All together, our results suggest a novel mechanism of reducing accumulation of monocytes at inflammation sites by disruption of JAM-C–mediated monocyte retention. Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, we show that blockade of JAM-B/-C interaction reduced monocyte numbers in the extravascular compartment through increased reverse transmigration rather than by reduced transmigration. This was confirmed in vivo, showing that an anti-JAM-C antibody reduced the number of monocytes in inflammatory tissue and increased the number of monocytes with a reverse-transmigratory phenotype in the peripheral blood. All together, our results suggest a novel mechanism of reducing accumulation of monocytes at inflammation sites by disruption of JAM-C-mediated monocyte retention.Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, we show that blockade of JAM-B/-C interaction reduced monocyte numbers in the extravascular compartment through increased reverse transmigration rather than by reduced transmigration. This was confirmed in vivo, showing that an anti-JAM-C antibody reduced the number of monocytes in inflammatory tissue and increased the number of monocytes with a reverse-transmigratory phenotype in the peripheral blood. All together, our results suggest a novel mechanism of reducing accumulation of monocytes at inflammation sites by disruption of JAM-C-mediated monocyte retention. |
| Author | Miljkovic-Licina, Marijana Imhof, Beat A. Nourshargh, Sussan Ody, Christiane Scheiermann, Christoph Aurrand-Lions, Michel Bradfield, Paul F. Rainger, G. Ed Nash, Gerard B. Luscinskas, Francis W. |
| Author_xml | – sequence: 1 givenname: Paul F. surname: Bradfield fullname: Bradfield, Paul F. organization: Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland – sequence: 2 givenname: Christoph surname: Scheiermann fullname: Scheiermann, Christoph organization: Faculty of Medicine, Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London, United Kingdom – sequence: 3 givenname: Sussan surname: Nourshargh fullname: Nourshargh, Sussan organization: Faculty of Medicine, Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London, United Kingdom – sequence: 4 givenname: Christiane surname: Ody fullname: Ody, Christiane organization: Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland – sequence: 5 givenname: Francis W. surname: Luscinskas fullname: Luscinskas, Francis W. organization: Department of Pathology, Center for Excellence in Vascular Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA – sequence: 6 givenname: G. Ed surname: Rainger fullname: Rainger, G. Ed organization: The Centre for Cardiovascular Sciences, Centre for Immune Regulation and the Medical Research Council (MRC) Centre, The University of Birmingham, Birmingham, United Kingdom – sequence: 7 givenname: Gerard B. surname: Nash fullname: Nash, Gerard B. organization: The Centre for Cardiovascular Sciences, Centre for Immune Regulation and the Medical Research Council (MRC) Centre, The University of Birmingham, Birmingham, United Kingdom – sequence: 8 givenname: Marijana surname: Miljkovic-Licina fullname: Miljkovic-Licina, Marijana organization: Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland – sequence: 9 givenname: Michel surname: Aurrand-Lions fullname: Aurrand-Lions, Michel organization: Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland – sequence: 10 givenname: Beat A. surname: Imhof fullname: Imhof, Beat A. email: beat.imhof@medecine.unige.ch organization: Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland |
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| Keywords | Monocyte Leukocyte Rodentia Cell adhesion molecule Inflammation Endothelium In vivo Cell motility Junctional adhesion molecule C Vertebrata Mammalia Mouse Animal Cell migration |
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| SubjectTerms | Animals Antibodies - immunology Biological and medical sciences Blood Platelets - metabolism Cell Adhesion Cell Adhesion Molecules - genetics Cell Adhesion Molecules - immunology Cell Adhesion Molecules - metabolism Cell Movement Cells, Cultured Endothelial Cells - metabolism Fundamental and applied biological sciences. Psychology Humans Immunobiology Inflammation Inflammation - metabolism Inflammation - pathology Junctional Adhesion Molecules Mice Mice, Transgenic Molecular and cellular biology Monocytes - cytology Monocytes - metabolism Phenotype |
| Title | JAM-C regulates unidirectional monocyte transendothelial migration in inflammation |
| URI | https://dx.doi.org/10.1182/blood-2007-03-078733 https://www.ncbi.nlm.nih.gov/pubmed/17625065 https://www.proquest.com/docview/68293371 https://pubmed.ncbi.nlm.nih.gov/PMC1988941 |
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