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Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes
CD16(+) monocytes represent 5–10% of peripheral blood monocytes in normal individuals and are dramatically expanded in several pathological conditions including sepsis, human immunodeficiency virus 1 infection, and cancer. CD16(+) monocytes produce high levels of proinflammatory cytokines and may re...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193954/ https://www.ncbi.nlm.nih.gov/pubmed/12810688 http://dx.doi.org/10.1084/jem.20022156 |
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author | Ancuta, Petronela Rao, Ravi Moses, Ashlee Mehle, Andrew Shaw, Sunil K. Luscinskas, F. William Gabuzda, Dana |
author_facet | Ancuta, Petronela Rao, Ravi Moses, Ashlee Mehle, Andrew Shaw, Sunil K. Luscinskas, F. William Gabuzda, Dana |
author_sort | Ancuta, Petronela |
collection | PubMed |
description | CD16(+) monocytes represent 5–10% of peripheral blood monocytes in normal individuals and are dramatically expanded in several pathological conditions including sepsis, human immunodeficiency virus 1 infection, and cancer. CD16(+) monocytes produce high levels of proinflammatory cytokines and may represent dendritic cell precursors in vivo. The mechanisms that mediate the recruitment of CD16(+) monocytes into tissues remain unknown. Here we investigate molecular mechanisms of CD16(+) monocyte trafficking and show that migration of CD16(+) and CD16(−) monocytes is mediated by distinct combinations of adhesion molecules and chemokine receptors. In contrast to CD16(−) monocytes, CD16(+) monocytes expressed high CX3CR1 and CXCR4 but low CCR2 and CD62L levels and underwent efficient transendo-thelial migration in response to fractalkine (FKN; FKN/CX3CL1) and stromal-derived factor 1α (CXCL12) but not monocyte chemoattractant protein 1 (CCL2). CD16(+) monocytes arrested on cell surface–expressed FKN under flow with higher frequency compared with CD16(−) monocytes. These results demonstrate that FKN preferentially mediates arrest and migration of CD16(+) monocytes and suggest that recruitment of this proinflammatory monocyte subset to vessel walls via the CX3CR1-FKN pathway may contribute to vascular and tissue injury during pathological conditions. |
format | Text |
id | pubmed-2193954 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21939542008-04-11 Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes Ancuta, Petronela Rao, Ravi Moses, Ashlee Mehle, Andrew Shaw, Sunil K. Luscinskas, F. William Gabuzda, Dana J Exp Med Article CD16(+) monocytes represent 5–10% of peripheral blood monocytes in normal individuals and are dramatically expanded in several pathological conditions including sepsis, human immunodeficiency virus 1 infection, and cancer. CD16(+) monocytes produce high levels of proinflammatory cytokines and may represent dendritic cell precursors in vivo. The mechanisms that mediate the recruitment of CD16(+) monocytes into tissues remain unknown. Here we investigate molecular mechanisms of CD16(+) monocyte trafficking and show that migration of CD16(+) and CD16(−) monocytes is mediated by distinct combinations of adhesion molecules and chemokine receptors. In contrast to CD16(−) monocytes, CD16(+) monocytes expressed high CX3CR1 and CXCR4 but low CCR2 and CD62L levels and underwent efficient transendo-thelial migration in response to fractalkine (FKN; FKN/CX3CL1) and stromal-derived factor 1α (CXCL12) but not monocyte chemoattractant protein 1 (CCL2). CD16(+) monocytes arrested on cell surface–expressed FKN under flow with higher frequency compared with CD16(−) monocytes. These results demonstrate that FKN preferentially mediates arrest and migration of CD16(+) monocytes and suggest that recruitment of this proinflammatory monocyte subset to vessel walls via the CX3CR1-FKN pathway may contribute to vascular and tissue injury during pathological conditions. The Rockefeller University Press 2003-06-16 /pmc/articles/PMC2193954/ /pubmed/12810688 http://dx.doi.org/10.1084/jem.20022156 Text en Copyright © 2003, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Ancuta, Petronela Rao, Ravi Moses, Ashlee Mehle, Andrew Shaw, Sunil K. Luscinskas, F. William Gabuzda, Dana Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes |
title | Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes |
title_full | Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes |
title_fullStr | Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes |
title_full_unstemmed | Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes |
title_short | Fractalkine Preferentially Mediates Arrest and Migration of CD16(+) Monocytes |
title_sort | fractalkine preferentially mediates arrest and migration of cd16(+) monocytes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193954/ https://www.ncbi.nlm.nih.gov/pubmed/12810688 http://dx.doi.org/10.1084/jem.20022156 |
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