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Phorbol esters cause sequential activation and deactivation of complement receptors on polymorphonuclear leukocytes
Journal of Immunology (Baltimore, Md. : 1950)
|March 1, 1986
Summary
Phorbol myristate acetate (PMA) initially boosts immune cell receptor activity for phagocytosis but later reduces it. This suggests receptor activation involves phosphorylation and deactivation involves dephosphorylation.
Area of Science:
- Immunology
- Cell Biology
Background:
- Polymorphonuclear leukocytes (PMN) are crucial immune cells.
- Receptors for complement fragments C3b/C3bi and Fc receptors play key roles in phagocytosis.
- Phorbol myristate acetate (PMA) is a known activator of PMNs.
Purpose of the Study:
- To investigate the biphasic effects of PMA on C3b/C3bi and Fc receptors in human PMNs.
- To explore the role of protein phosphorylation and dephosphorylation in PMA-induced receptor modulation.
Main Methods:
- Human PMNs were treated with PMA for varying durations (10 min and 60 min).
- Phagocytosis assays were performed using erythrocytes coated with C3b/C3bi or IgG.
- PMNs were loaded with thiophosphate (thioP) to create phosphatase-resistant phosphorylated proteins.
Main Results:
- PMA treatment initially enhanced C3b/C3bi receptor-mediated phagocytosis but subsequently reduced it.
- PMA reduced Fc receptor-mediated phagocytosis and the binding affinity for immune complexes.
- Thiophosphate loading prevented PMA-induced deactivation of C3 and Fc receptors.
Conclusions:
- PMA induces qualitative changes in C3 and Fc receptors, leading to sequential activation and deactivation.
- Receptor activation is mediated by phosphorylation.
- Receptor deactivation is mediated by dephosphorylation.