Fractalkine preferentially mediates arrest and migration of CD16+ monocytes

Petronela Ancuta, Ravi Rao, Ashlee Moses, Andrew Mehle, Sunil K. Shaw, F. William Luscinskas, Dana Gabuzda

Research output: Contribution to journalArticlepeer-review

471 Scopus citations


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 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.

Original languageEnglish (US)
Pages (from-to)1701-1707
Number of pages7
JournalJournal of Experimental Medicine
Issue number12
StatePublished - Jun 16 2003


  • Cell adhesion
  • Chemokine receptors
  • Chemokines
  • Chemotaxis
  • Inflammation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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