Genetic deficiency of CD16, the low-affinity receptor for immunoglobulin G, has no impact on the functional capacity of polymorphonuclear neutrophils.

BACKGROUND: Of the three receptors for immunoglobulin G (IgG), the low-affinity receptor CD16 is constitutively expressed on polymorphonuclear neutrophils (PMNs), monocytes and NK-cells. CD16 participates in various effector functions, notably phagocytosis of opsonized particles or of immune complexes, and in antibody-dependent cellular cytotoxicity (ADCC). In the present study we report a case of total CD16 deficiency on PMNs and monocytes.
DESIGN: Polymorphonuclear neutrophils, monocytes and NK-cells were analyzed for surface-receptor expression by cytofluorometry and laser scan microscopy. Moreover, CD16-specific mRNA was assessed by RT-PCR. As functional parameters, phagocytosis of opsonized bacteria was tested, as was superoxide production.
RESULTS: Polymorphonuclear neutrophils and monocytes totally deficient in CD16 were detected by chance in an apparently healthy individual. Further analysis revealed that two more members of his family, his father and sister, were also deficient in CD16. All were healthy and there was no evidence of an increased frequency, or of exceptionally severe or persistent infections. Despite the lack of CD16, phagocytosis of antibody-coated bacteria was within the normal range, as was the superoxide production.
CONCLUSION: Deficiency of CD16 does not compromise the host defence. Apparently, the other receptors for IgG, CD32 and CD64, can compensate for the lack of CD16.