Up-regulation of the iC3b receptor (CR3) is neither necessary nor sufficient to promote neutrophil aggregation

M. R. Philips, J. P. Buyon, R. Winchester, G. Weissmann, S. B. Abramson

Research output: Contribution to journalArticlepeer-review

138 Scopus citations

Abstract

The iC3b receptor (CR3) is required for neutrophil adhesive functions, including homotypic aggregation. Because stimuli that enhance neutrophil adhesion also induce up-regulation of surface CR3, it is widely held that these two responses are causally related. We have dissociated CR3 display (immunofluorescence) from CR3 function (aggregation). Neutrophils isolated at 4°C and rewarmed to 37°C up-regulated surface CR3 twofold, but did not aggregate. The kinetics of FMLP-induced CR3 up-regulation were discordant with those of aggregation. In the absence of extracellular divalent cations, CR3 expression increased twofold after exposure to FMLP, but neutrophils did not aggregate. FMLP elicited 3.5-fold more aggregation than the ionophore A23187, yet less than one-half as much CR3 up-regulation. 3 mM sodium salicylkate inhibited aggregation 55 ± 4%, but had no effect on CR3 up-regulation. Conversely, 1 mM tetracaine complewtely inhibited CR3 up-regulation, while significantly enhancing aggregation. Neutroplasts expressed CR3, but did not up-regulate the receptor; in contrast, FMLP induced CR3-dependent aggregation of neutroplasts. We conclude that, although constitutive surface CR3 is required for neutrophil aggregation, the up-regulation of CR3 is neither necessary nor sufficient to promote cell-cell adhesion.

Original languageEnglish
Pages (from-to)495-501
Number of pages7
JournalJournal of Clinical Investigation
Volume82
Issue number2
DOIs
StatePublished - 1988
Externally publishedYes

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