Abstract
Neutrophils are best known for their critical role in host defense, for which they utilize multiple innate immune mechanisms, including microbe-associated pattern recognition, phagocytosis, production of reactive oxygen species, and the release of potent proteases, mediators, antimicrobials, and neutrophil extracellular traps. Beyond their well-established contribution to innate immunity, neutrophils were more recently reported to interact with various other cell types, including cells from the adaptive immune system, thereby enabling neutrophils to tune the overall immune response of the host. Neutrophils express different receptors for IgG antibodies (Fcγ receptors), which facilitate the engulfment of IgG-opsonized microbes and trigger cell activation upon cross-linking of several receptors. Indeed, FcγRs (via IgG antibodies) confer neutrophils with a key feature of the adaptive immunity: an antigen-specific cell response. This review summarizes the expression and function of FcγRs on human neutrophils in health and disease and how they are affected by polymorphisms in the FCGR loci. Additionally, we will discuss the role of neutrophils in providing help to marginal zone B cells for the production of antibodies, which in turn may trigger neutrophil effector functions when engaging FcγRs.
Highlights
Neutrophils are key players of the innate immune response
The tight control of neutrophil homeostasis is critical for the organism as many of their effector functions [i.e., production of reactive oxygen species (ROS), release of neutrophil extracellular traps (NETs), or granules containing potent proteases and lipophosphatases [9]] bare the potential to be deleterious for the host and damage surrounding tissues and organs
This study provides a mechanistic explanation for the observation made earlier that FcγRIIA appears to have a lower affinity for IgG on resting neutrophils than on preactivated ones
Summary
Neutrophils are key players of the innate immune response. They are the most abundant leukocytes in the human blood (4.5–11 × 103/mm3). This cell activation requires co-engagement of another neutrophil FcγR, FcγRIIA via the Fc portion of the intact antibody [33]. The authors report that FcγRIIIA engagement on neutrophils from FcγRIIIB-deficient and normal individuals efficiently triggers cell activation and mediates phagocytosis of IgG-opsonized beads that could not be blocked by anti-FcγRIIA F(ab′)2 fragments [51].
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