Relevance of IgG receptor IIIb (CD16) polymorphism to handling of Porphyromonas gingivalis: implications for the pathogenesis of adult periodontitis

Polymorphonuclear neutrophils (PMNs) are essential in host defense against periodontopathic bacteria such as Porphyromonas gingivalis. The uptake of immunoglobulin G (IgG)‐opsonized bacteria via IgG Fc receptors (FcγR) on PMN constitutes a central defense mechanism in periodontium. FcγRIIIb is the most abundantly expressed FcγR on PMN and is functionally polymorphic. The FcγRIIIb‐NA1 and IIIb‐NA2 allotypes interact differently with IgG1‐ and IgG3‐opsonized particles. We recently showed recurrence rates of adult periodontitis (AP) to be higher in patients carrying at least 1 FcγRIIIb‐NA2 allele. In this study we evaluated the functional relevance of the FcγRIIIb polymorphism to anti‐P. gingivalis PMN effector functions. Our results showed FcγRIIIb‐NA2‐carrying PMN from both patients with AP and healthy controls to be less efficient in phagocytosis and induction of oxidative burst upon interaction with IgG1‐ and IgG3‐opsonized P. gingivalis. These functional differences between FcγRIIIb‐NA1 and IIIb‐NA2 were observed in the presence of CD32‐blocking antibody fragments, but not upon blocking CD16. Moreover, PMNs from AP patients exhibited increased FcγRIIIb‐allelic differences in IgG3‐induced oxidative burst compared to control PMNs. These results support the concept that FcγRIIIb heterogeneity may influence the clinical course of AP.