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CD66‐dependent neutrophil activation: a possible mechanism for vascular selectin‐mediated regulation of neutrophil adhesion
Author(s) -
Stocks S. Craig,
Kerr Michael A.,
Haslett Christopher,
Dransfield Ian
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.1.40
Subject(s) - integrin , respiratory burst , p selectin , immunology , priming (agriculture) , biology , cd18 , effector , selectin , l selectin , cell adhesion molecule , receptor , microbiology and biotechnology , platelet activation , biochemistry , platelet , botany , germination
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 β 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 β 2 ‐integrin up‐regulation and 70% loss of L‐selectin, whereas only low‐level up‐regulation of the β 2 ‐integrins, without loss of L‐selectin, occurred with anti‐CEA Ig. Anti‐CEA F(ab') 2 fragments and whole Ig augmented β 2 ‐integrin‐dependent adhesion. Anti‐CEA Ig‐induced β 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. J. Leukoc. Biol. 58: 40–48; 1995.