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Cited by 75Monoclonal and Polyclonal Antibodies ResearchPhagocytosis and Immune RegulationImmune Response and Inflammation

Fcγ receptor-mediated activation of phospholipase D regulates macrophage phagocytosis of IgG-opsonized particles

Kusner, David J, Hall, Clifton F, Jackson, Stephen·1999·The Journal of Immunology
DOI 10.4049/jimmunol.162.4.2266
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Abstract

Receptors for the Fc portion of IgG (FcγRs) integrate the innate and acquired components of immunity by coupling the specific recognition of IgG Abs to the activation of phagocytic leukocytes. Knowledge of the molecular mechanisms that regulate phagocyte stimulation by FcγRs may permit therapeutic modulation to augment immunoprotective aspects and minimize damage to host tissues in diverse inflammatory diseases. Since phospholipase D (PLD) has been linked to the stimulation of cytotoxic leukocyte responses, we characterized FcγR-dependent activation of PLD in human macrophages. IgG-coated SRBCs (EIgG) stimulated a 9.4-fold increase in PLD activity compared with SRBCs treated with control Ab (p < 0.001), determined by formation of the PLD-specific product phosphatidylethanol in the presence of 0.5% ethanol. Levels of phosphatidic acid, the physiologic product of PLD-mediated catalyzis, were significantly increased in the absence of ethanol (6.4-fold, p < 0.001). PLD activity was also stimulated by immune complex-coated latex beads or cross-linking of Abs specific for FcγRI, FcγRII, or FcγRIII. Phagocytosis of EIgG was reduced by two inhibitors of PLD-mediated signaling, 2,3-diphosphoglycerate or 1-butanol. Addition of purified PLD restored control levels of phagocytosis in cells in which endogenous PLD was inhibited. The tyrosine kinase inhibitors genistein and herbimycin A caused concordant reductions in FcγR-stimulated PLD activity and phagocytosis. These studies demonstrate…

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  • The accumulation of DAG results, at least in part, from activation of PLC, although a contribution of phospholipase D and phosphatidate phosphohydrolase is also possible.

    “The latter results, at least in part, from activation of PLC, although a contribution of phospholipase D and phosphatidate phosphohydrolase is also possible (Kusner et al. 1999).”

    From Localized Biphasic Changes in Phosphatidylinositol-4,5-Bisphosphate at Sites of Phagocytosis (2000) · cites this paper as Kusner et al. 1999

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Authors
Kusner, D. J., Hall, C. F., & Jackson, S.
Affiliations
University of Iowa (US)
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
1999-02
Volume
162
Issue
4
Pages
2266-2274
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.162.4.2266
OpenAlex
W4313341524
Cited by
75
References
45
Citations by year
2025: 2 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 5 · 2018: 1 · 2016: 2 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
6.08
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
The Journal of Immunology (publishedVersion)
Topics
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Monoclonal and Polyclonal Antibodies Research
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
Fc gamma receptor, phospholipase D, macrophage phagocytosis, IgG opsonization, tyrosine kinase signaling, FcγRI, FcγRII, FcγRIII, immune complexes, phosphatidic acid, 2,3-diphosphoglycerate, genistein, herbimycin A, innate immunity

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