Chronic HIV-1 Infection Alters the Cellular Distribution of Fc γRIIIa and the Functional Consequence of the FcγRIIIa-F158V Variant

In conclusion, our findings demonstrate that in the presence of an HIV-1 infection, the cellular distribution of FcγRIIIa is altered and that the functional consequence of FcγRIIIa variant is affected. Importantly, it underscores the need to characterize FcγR expression, cellular distribution and functional consequences of FcγR genetic variants within a specific environment or disease state. Introduction Receptors for the Fc domain of immunoglobulin G (IgG), so called Fc gamma receptors (FcγRs), link the specificity of IgG with potent effector functions of the innate immune system. FcγRs comprise a family of activating (FcγRI, FcγRIIa, and FcγRIIIa) and inhibiting (FcγRIIb) receptors that are differentially expressed on innate immune cells such as natural killer (NK) cells, monocytes, dendritic cells, neutrophils, and granulocytes (1–3). During an infection, these receptors play an important role in activating IgG-induced protective inflammatory processes and regulating immune responses (4–7). Increasing evidence support an important role for FcγR-mediated effector functions, in particular antibody-dependent cellular cytotoxicity (ADCC), in HIV-1-specific immunity (6, 8). In adults, ADCC has been associated with a reduced risk of HIV-1 acquisition in the RV144 vaccine trial, whereas in infants born to HIV-1 infected mothers, passively acquired ADCC activity associate...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research