The Journal of Experimental Medicine
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Published 4 October 2004. doi:10.1084/jem.20040501
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 7, 835-846
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C1q Governs Deposition of Circulating Immune Complexes and Leukocyte Fc{gamma} Receptors Mediate Subsequent Neutrophil Recruitment

Tracy Stokol1, Peter O'Donnell1, Ling Xiao1, Sara Knight1, George Stavrakis1, Marina Botto3, Ulrich H. von Andrian2, and Tanya N. Mayadas1

1 Vascular Research Division, Department of Pathology, Brigham and Women's Hospital
2 The Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, MA 02115
3 Rheumatology Section, Faculty of Medicine, Imperial College, London SW7 2AZ, UK

Address correspondence to Tanya N. Mayadas, Dept. of Pathology, Brigham and Women's Hospital, 77 Ave. Louis Pasteur, 7520 NRB, Boston, MA 02115. Phone: (617) 525-4336; Fax: (617) 525-4333; email: tmayadas{at}rics.bwh.harvard.edu

Inflammation induced by circulating immunoglobulin G–immune complexes (ICs) characterizes many immune-mediated diseases. In this work, the molecular requirements for the deposition of circulating ICs and subsequent acute leukocyte recruitment in mice were elucidated. We show that after intravenous injection, preformed soluble ICs are rapidly deposited in the postcapillary venules of the cremaster microcirculation, secondary to increased vascular permeability. This deposition is dependent on complement C1q. IC deposition is associated with leukocyte recruitment. Leukocyte rolling, which is mediated by P-selectin in the exteriorized cremaster muscle, is not further increased in response to ICs. In contrast, leukocyte rolling velocity is significantly decreased and leukocyte adhesion is significantly increased in the presence of ICs. The IC-mediated slow leukocyte rolling velocity and subsequent adhesion and emigration are dependent on Fc{gamma} receptors (Fc{gamma}Rs), particularly Fc{gamma}RIII, with complement C3 and C5 having no detectable role. These studies suggest a regulatory mechanism of IC deposition and leukocyte trafficking in IC-mediated inflammation requiring C1q and Fc{gamma}Rs in sequential, noninteracting roles.

Key Words: antigen–antibody complex • Fc receptors • animal models • complement 1q • microscopy

Abbreviations used in this paper: Ab, antibody; Ag, antigen; EC, endothelial cell; IC, immune complex; ICAM, intercellular adhesion molecule; IHC, immunohistochemistry; IVM, intravital microscopy; R/F, rolipram and forskolin; VCAM, vascular cell adhesion molecule; VEGF, vascular endothelial growth factor.


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