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(Journal of Leukocyte Biology. 2006;80:1156-1164.)
© 2006 by Society for Leukocyte Biology

CD16⁺ monocytes produce IL-6, CCL2, and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing endothelial cells

Petronela Ancuta^*,, Jianbin Wang^*, and Dana Gabuzda^*,,1

^* Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, and Departments of
Pathology and
Neurology, Harvard Medical School, Boston, Massachusetts, USA

¹ Correspondence: Dana-Farber Cancer Institute, 44 Binney St., JFB 816, Boston, MA 02115. E-mail: dana_gabuzda{at}dfci.harvard.edu

ABSTRACT

The CD16⁺ subset of peripheral blood monocytes (Mo) is expanded dramatically during inflammatory conditions including sepsis, HIV-1 infection, and cancer. CD16⁺ express high levels of CX3CR1, which mediates arrest onto CX3CL1-expressing endothelial cells (EC) under flow conditions. In contrast, attachment of CD16^– Mo onto cytokine-activated EC is independent of CX3CL1. Here, we investigate the ability of CD16⁺ and CD16^– Mo to produce proinflammatory cytokines upon interaction with CX3CL1-expressing HUVEC. We demonstrate that CD16⁺ but not CD16^– Mo produce high levels of IL-6, CCL2, and matrix metalloproteinase (MMP)-9 when cocultured with TNF/IFN--activated HUVEC or nonactivated HUVEC expressing CX3CL1. Furthermore, supernatants from Mo cocultured with cytokine-activated HUVEC induce neuronal death in vitro. These results suggest that membrane-bound CX3CL1 stimulates production of IL-6, CCL2, and MMP-9 by CD16⁺ Mo, likely via engagement of CX3CR1. Thus, expansion of CD16⁺ Mo and their accumulation onto CX3CL1-expressing EC may result in recruitment of Mo and T cell subsets at sites of inflammation in response to CCL2, IL-6-induced cell activation and/or differentiation, and MMP-9-mediated vascular and tissue injury.

Key Words: vascular injury • chemokines • CX3CR1 • neurotoxicity • neurogeneration

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