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Fc gamma RIII mediates neutrophil recruitment to immune complexes. a mechanism for neutrophil accumulation in immune-mediated inflammation.

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 Fc gamma receptor IIIB (Fc gamma RIIIB), and the beta(2) integrins are additionally required for the subsequent shear-resistant adhesion. The attachment function of Fc gamma RIIIB 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, Fc gamma RIII-deficient mice had a significant reduction in neutrophil recruitment. Thus, the interaction of immune complexes with Fc gamma RIII may mediate early neutrophil recruitment in immune complex-mediated inflammation.

journal_name

Immunity

journal_title

Immunity

authors

Coxon A,Cullere X,Knight S,Sethi S,Wakelin MW,Stavrakis G,Luscinskas FW,Mayadas TN

doi

10.1016/s1074-7613(01)00150-9

keywords:

subject

Has Abstract

pub_date

2001-06-01 00:00:00

pages

693-704

issue

6

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(01)00150-9

journal_volume

14

pub_type

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