Date of this Version
Journal of Immunology
Phosphorylation of G protein-coupled receptors and the subsequent recruitment of β-arrestin play an important role in desensitization of receptor-mediated responses, including degranulation in leukocytes. In this study, we report that receptor phosphorylation also provides a stimulatory signal for CCR ligand 2 (CCL2) production. C3a stimulated degranulation in a basophilic leukemia RBL-2H3 cell expressing wildtype C3aR or a phosphorylation-deficient mutant (ΔST-C3aR). In contrast, C3a caused CCL2 production only in C3aR but not eΔST-C3aR cells. Furthermore, overexpression of G protein-coupled receptor kinase 2 resulted in enhancement of both ligand-induced receptor phosphorylation and CCL2 production but inhibition of degranulation. Agonist activation of C3aR, but not ΔST-C3aR, led to the translocation of green fluorescent protein tagged β-arrestin 2 from the cytoplasm to the plasma membrane. These data demonstrate that receptor phosphorylation, which provides a turn off signal for degranulation, is essential for CCL2 production.
Ahamed, J., Haribabu, B., & Ali, H. (2001). Cutting Edge: Differential Regulation of Chemoattractant Receptor-Induced Degranulation and Chemokine Production by Receptor Phosphorylation. Journal of Immunology, 167 (7), 3559-3563. http://dx.doi.org/10.4049/jimmunol.167.7.3559
Date Posted: 08 December 2022
This document has been peer reviewed.