Résumé
Neutrophils are innate immune cells with immunomodulatory functions. Using a murine retroviral model, we previously demonstrated their role in promoting protective immunity during antibody therapy through Fc-Fcγ receptor (FcγR) interactions. Here, we investigated neutrophil activation and FcγR regulation in the context of HIV-1 infection and antibody-based therapies. Neutrophils from healthy donors (HD) and people living with HIV-1 (PLWH) were stimulated with TLR ligands, free HIV-1, immune complexes (ICs) formed with broadly neutralizing antibodies (bNAbs), or pro-inflammatory cytokines. Neutrophils displayed stimulus-dependent cytokine and chemokine responses. HD neutrophils showed limited activation and FcγR modulation in response to free HIV-1 or IC compared with TLR agonists or cytokines. Conversely, PLWH neutrophils exhibited heightened responsiveness to HIV-associated stimuli, with increased secretion of IFNγ, CXCL1, CCL2, CCL3, and CCL4, along with elevated expression of activating FcγRs and activation markers. These findings highlight the influence of the inflammatory milieu on neutrophil function and FcγR regulation during HIV-1 infection.