The Journal of Experimental Medicine
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Published 16 June 2003. doi:10.1084/jem.20022156
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© Rockefeller University Press, 0022-1007/2003/6/1701 $5.00
The Journal of Experimental Medicine, Volume 197, Number 12, 1701-1707

Fractalkine Preferentially Mediates Arrest and Migration of CD16+ Monocytes

Petronela Ancuta1, Ravi Rao2, Ashlee Moses3, Andrew Mehle1, Sunil K. Shaw2, F. William Luscinskas2 and Dana Gabuzda1

1 Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute
2 Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115
3 Vaccine and Gene Therapy Institute, Oregon Health & Sciences University, Beaverton, OR 97006

Address correspondence to Dana Gabuzda, Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, JFB 816, Boston, MA 02115. Phone: 617-632-2154; Fax: 617-632-3113; E-mail: dana_gabuzda{at}dfci.harvard.edu

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 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.

Key Words: chemokines • chemokine receptors • chemotaxis • cell adhesion • inflammation


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