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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...

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Autores principales: Ancuta, Petronela, Rao, Ravi, Moses, Ashlee, Mehle, Andrew, Shaw, Sunil K., Luscinskas, F. William, Gabuzda, Dana
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2003
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.
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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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