CD66-dependent neutrophil activation: a possible mechanism for vascular selectin-mediated regulation of neutrophil adhesion
| Autor: | Ian Dransfield, Christopher Haslett, S C Stocks, Michael A. Kerr |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Integrins
Time Factors Neutrophils Immunology Integrin Molecular Sequence Data Priming (immunology) Inflammation In Vitro Techniques Neutrophil Activation Antigens CD medicine Cell Adhesion Immunology and Allergy Humans Amino Acid Sequence L-Selectin Cell adhesion Serum Albumin Respiratory Burst biology CD11 Antigens Fibrinogen Cell Biology Molecular biology Antigens Differentiation Respiratory burst Carcinoembryonic Antigen N-Formylmethionine Leucyl-Phenylalanine CD18 Antigens Luminescent Measurements biology.protein L-selectin medicine.symptom Antibody Cell Adhesion Molecules Selectin Protein Binding |
| Zdroj: | Journal of leukocyte biology. 58(1) |
| ISSN: | 0741-5400 |
| Popis: | 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 β2-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 β2-integrin up-regulation and 70% loss of L-selectin, whereas only low-level up-regulation of the β2-integrins, without loss of L-selectin, occurred with anti-CEA Ig. Anti-CEA F(ab’)2 fragments and whole Ig augmented β2-integrin-dependent adhesion. Anti-CEA Ig-induced β2-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. |
| Databáze: | OpenAIRE |
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