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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2003-6-17
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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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-10400787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-10805752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-10811011,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-10942707,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11200054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11282167,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11287620,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11376329,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11561000,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11696600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11696601,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11698220,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11733377,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11825560,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11907116,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-11978078,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-12044982,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-12186843,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-12569158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-12600915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-1825635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-2179952,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-8566032,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-8683134,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-8854561,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-9024663,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-9078201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-9390561,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12810688-9782118
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/CX3CL1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CX3CR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CX3CL1,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CX3C,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
197
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1701-7
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12810688-Antibodies, Monoclonal,
pubmed-meshheading:12810688-Cell Cycle,
pubmed-meshheading:12810688-Cell Movement,
pubmed-meshheading:12810688-Chemokine CX3CL1,
pubmed-meshheading:12810688-Chemokines, CX3C,
pubmed-meshheading:12810688-Humans,
pubmed-meshheading:12810688-Lymphocyte Subsets,
pubmed-meshheading:12810688-Membrane Proteins,
pubmed-meshheading:12810688-Monocytes,
pubmed-meshheading:12810688-Phenotype,
pubmed-meshheading:12810688-Protein Binding,
pubmed-meshheading:12810688-Receptors, Chemokine,
pubmed-meshheading:12810688-Receptors, IgG
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pubmed:year |
2003
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pubmed:articleTitle |
Fractalkine preferentially mediates arrest and migration of CD16+ monocytes.
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pubmed:affiliation |
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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