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Originally published online as doi:10.1189/jlb.0607421 on March 27, 2008

Published online before print March 27, 2008
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(Journal of Leukocyte Biology. 2008;83:1423-1430.)
© 2008 by Society for Leukocyte Biology

Role of TNF priming and adhesion molecules in neutrophil recruitment to intravascular immune complexes

Michael Lauterbach, Peter O'Donnell, Kenichi Asano and Tanya N. Mayadas1

Center of Excellence in Vascular Biology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA

1Correspondence: Center of Excellence in Vascular Biology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, New Research Building 7520, Boston, MA 02115, USA. E-mail: tmayadas{at}rics.bwh.harvard.edu

Neutrophils play an important role in immune complex (IC)-mediated diseases, but the mechanisms underlying their recruitment to sites of IC deposition remain largely undefined. Furthermore, neutrophils encounter cytokines that prime their effector functions, yet the physiological relevance of priming to neutrophil functions is unclear. Using intravital microscopy, we demonstrate that TNF treatment of neutrophils ex vivo significantly increased their adhesion in a model of intravascular ICs deposited in the cremaster muscle. Notably, TNF priming had no effect on neutrophil adhesion in the absence of ICs. Analyses of relevant knockout mice and neutrophil reconstitution revealed a critical role for Fc{gamma}Rs and the CD18 integrin Mac-1 in IC-mediated neutrophil adhesion. Furthermore, ICAM-1, a major Mac-1 ligand constitutively expressed on unactivated endothelium, significantly contributed to this process. These data suggest that TNF priming promotes Fc{gamma}R interaction with intravascular ICs, leading to the binding of Mac-1 to ICAM-1 and subsequent neutrophil arrest.

Key Words: adhesion molecules • Fc receptors • cytokines • cell trafficking




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