Neutrophil FcγRI expression as a determinant of oxidative responses in human blood
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Purpose
Neutrophils express Fc receptors on their surface to trap immune complexes. While the implication of FcγRIIa and FcγRIIIb have extensively been studied in that context, that of FcγRI remains elusive. Recently, aggregated IgGs have been shown to induce rapid FcγRI upregulation and reactive oxygen species (ROS) generation, but the biological relevance of this process is still unclear.
Methods
Blood samples were obtained from healthy volunteers and patients with lupus. Aggregated IgGs were prepared as a model of immune complex. FcγRs’ surface expression on circulating leukocytes and on freshly isolated neutrophils was measured by flow cytometry. ROS production was monitored with luminol-based chemiluminescence.
Results
Incubation of blood samples from healthy volunteers with aggregated IgGs rapidly upregulated the surface expression of FcγRI, predominantly on neutrophils. Stimulation of isolated neutrophils from healthy donors with aggregated IgGs resulted in the production of ROS in an FcγRI-dependent fashion. Cytochalasin B potentiated FcγRI expression and ROS production. Positive correlations between neutrophil FcγRI and ROS production were observed in resting blood from both healthy volunteers and lupus patients. In the lupus cohort, monocyte FcγRI also correlated with ROS production.
Conclusion
This study unveils a previously underappreciated role for neutrophil FcγRI in ROS production in both healthy individuals and patients with lupus, and identifies FcγRI as a potential biomarker of oxidative response.
