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pubmed-article:12810688pubmed:abstractTextCD16+ 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 transendothelial migration in response to fractalkine (FKN; FKN/CX3CL1) and stromal-derived factor 1 alpha (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.lld:pubmed
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pubmed-article:12810688pubmed:authorpubmed-author:SuyaHHlld:pubmed
pubmed-article:12810688pubmed:authorpubmed-author:GabuzdaDanaDlld:pubmed
pubmed-article:12810688pubmed:authorpubmed-author:ShawSunil KSKlld:pubmed
pubmed-article:12810688pubmed:authorpubmed-author:MehleAndrewAlld:pubmed
pubmed-article:12810688pubmed:authorpubmed-author:AncutaPetrone...lld:pubmed
pubmed-article:12810688pubmed:authorpubmed-author:MosesAshleeAlld:pubmed
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pubmed-article:12810688pubmed:volume197lld:pubmed
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pubmed-article:12810688pubmed:authorsCompleteYlld:pubmed
pubmed-article:12810688pubmed:pagination1701-7lld:pubmed
pubmed-article:12810688pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:12810688pubmed:articleTitleFractalkine preferentially mediates arrest and migration of CD16+ monocytes.lld:pubmed
pubmed-article:12810688pubmed:affiliationDepartment of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.lld:pubmed
pubmed-article:12810688pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12810688pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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