pubmed-article:12810688 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C0535298 | lld:lifeskim |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C0108747 | lld:lifeskim |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C1414555 | lld:lifeskim |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C0237477 | lld:lifeskim |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C0600210 | lld:lifeskim |
pubmed-article:12810688 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:12810688 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:12810688 | pubmed:dateCreated | 2003-6-17 | lld:pubmed |
pubmed-article:12810688 | pubmed:abstractText | 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 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:12810688 | pubmed:language | eng | lld:pubmed |
pubmed-article:12810688 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12810688 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12810688 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12810688 | pubmed:month | Jun | lld:pubmed |
pubmed-article:12810688 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:SuyaHH | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:GabuzdaDanaD | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:ShawSunil KSK | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:MehleAndrewA | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:AncutaPetrone... | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:MosesAshleeA | lld:pubmed |
pubmed-article:12810688 | pubmed:author | pubmed-author:LuscinskasF... | lld:pubmed |
pubmed-article:12810688 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12810688 | pubmed:day | 16 | lld:pubmed |
pubmed-article:12810688 | pubmed:volume | 197 | lld:pubmed |
pubmed-article:12810688 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12810688 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12810688 | pubmed:pagination | 1701-7 | lld:pubmed |
pubmed-article:12810688 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:12810688 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12810688 | pubmed:articleTitle | Fractalkine preferentially mediates arrest and migration of CD16+ monocytes. | lld:pubmed |
pubmed-article:12810688 | pubmed:affiliation | Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. | lld:pubmed |
pubmed-article:12810688 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12810688 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12810688 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:12810688 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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