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J Leukoc Biol. 1995 Jul;58(1):40-8.

CD66-dependent neutrophil activation: a possible mechanism for vascular selectin-mediated regulation of neutrophil adhesion.

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Department of Respiratory Medicine, University of Edinburgh Medical School, United Kingdom.


We have examined the role of CD66 in the modulation of neutrophil adhesion and effector function. Engagement of neutrophil CD66 with anti-carcinoembryonic antigen (anti-CEA) Ig results in activation-associated phenomena including shape change, activation of beta 2-integrins, and priming of the respiratory burst. Anti-CEA Ig-treated neutrophils underwent transient shape change distinct from that induced by formyl-Met-Leu-Phe (fMLP). fMLP stimulated beta 2-integrin up-regulation and 70% loss of L-selectin, whereas only low-level up-regulation of the beta 2-integrins, without loss of L-selectin, occurred with anti-CEA Ig. Anti-CEA F(ab')2 fragments and whole Ig augmented beta 2-integrin-dependent adhesion. Anti-CEA Ig-induced beta 2-integrin activation was transient, whereas fMLP-induced activation persisted longer. Although they did not cause a significant increase in respiratory burst activity, CEA Ig and F(ab')2 fragments of antibody primed neutrophils so that the subsequent fMLP-induced respiratory burst was significantly increased.

[Indexed for MEDLINE]

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