FcγRIII mediates neutrophil recruitment to immune complexes: A mechanism for neutrophil accumulation in immune-mediated inflammation

Angela Coxon, Xavier Cullere, Sara Knight, Sanjeev Sethi, Matthew W. Wakelin, George Stavrakis, Francis W. Luscinskas, Tanya N. Mayadas

Research output: Contribution to journalArticle

145 Scopus citations

Abstract

Neutrophil accumulation is a hallmark of immune complex-mediated inflammatory disorders. Current models of neutrophil recruitment envision the capture of circulating neutrophils by activated endothelial cells. We now demonstrate that immobilized immune complexes alone support the rapid attachment of neutrophils, under physiologic flow conditions. Initial cell tethering requires the low-affinity Fcγ receptor IIIB (FcγRIIIB), and the β2 integrins are additionally required for the subsequent shear-resistant adhesion. The attachment function of FcγRIIIB may be facilitated by its observed presentation on neutrophil microvilli. In vivo, in a model of acute antiglomerular basement membrane nephritis in which immune complexes are accessible to circulating neutrophils, FcγRIII-deficient mice had a significant reduction in neutrophil recruitment. Thus, the interaction of immune complexes with FcγRIII may mediate early neutrophil recruitment in immune complex-mediated inflammation.

Original languageEnglish (US)
Pages (from-to)693-704
Number of pages12
JournalImmunity
Volume14
Issue number6
DOIs
StatePublished - Jan 1 2001

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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