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Boireau, S.

Publications and source records attributed to Boireau, S..

2 recordsLinked to original sources
bioRxiv2026

Differential Effects of Distinct Type I Interferons and IFN Inducers on Fc Receptor landscape and myeloid cell function

Antiviral monoclonal antibodies (mAbs) rely on Fc-mediated effector functions, which depend on interactions with Fc receptors (FcRs) expressed on immune cells such as monocytes and dendritic cells (DCs). While combinations of antiviral mAbs with type I interferons (IFN-I) or IFN inducers are being explored to enhance therapeutic efficacy, the impact of these immunomodulators on FcR expression remains poorly understood. In this study, we investigated the effects of IFN-2, IFN-{beta}, and the IFN-inducer TAK-981 (a SUMOylation inhibitor) on FcR modulation and functional activation in human monocyte subsets and monocyte-derived DCs (moDCs). Using flow cytometry and imaging techniques, we mapped the expression of activating Fc{gamma}Rs (CD64, CD32A, CD16A) and neonatal FcR (FcRn) under steady-state and stimulated conditions. We found that IFN-I selectively downregulates CD16A expression in classical monocytes while preserving other FcRs, whereas TAK-981 reduces FcRn expression in classical monocytes without affecting CD16A. Additionally, IFN-{beta} and TAK-981 but not IFN-2, selectively enhanced Fc{gamma}RI expression in moDC. IFN-{beta} also induced a stronger maturation and functional activation program in monocytes and moDCs compared with IFN-2, whereas TAK-981 largely reproduced the IFN-{beta}-driven phenotype and secretory profile. Furthermore, we demonstrated that IFN-I signaling alters the spatial distribution of FcRs, with IFN-{beta} and TAK-981 promoting distinct redistribution patterns of Fc{gamma}Rs in monocytes and moDCs. These findings reveal a novel layer of FcR regulation, highlighting that IFN-I and IFN inducers differentially modulate FcR expression, localization, and functional activation in a cell-type- and stimulus-specific manner. Overall, this work provides a framework for understanding how IFN-I-based immunotherapies may influence Fc-mediated immune functions while preserving FcRn-dependent antibody persistence.

immunology↗
bioRxiv2025

Temporal dynamics of macrophages transcriptional profiles during zebrafish wound healing

Macrophages participate to wound healing by contributing to host defense and orchestrating inflammation and repair. They adapt dynamically to the wound microenvironment by adopting diverse polarization states, which are determinant of wound outcome, influencing whether healing is successful or becomes chronic. The zebrafish embryo, widely used for live imaging of immune responses, is a powerful model to study macrophage behavior after injury. However, the transcriptional landscape of polarized macrophages in this model during wound healing remains insufficiently characterized. Here, we employ bulk RNA sequencing to characterize macrophage transcriptional programs following tail fin wounding a robust model for studying sterile inflammation. Our findings reveal that zebrafish macrophages undergo large transcriptomic changes along different wound healing phases, particularly between 2 and 5 hours post-amputation, suggesting a fast reprogramming leading to different functional states. We further show that, at 2h, macrophages acquire a pro-inflammatory profile with a gene signature closed to M1 signature. At 5h, macrophages express genes involved in immunoregulation and healing associated with shutoff of pro-inflammatory pathways and the activation of glucose and glycogen metabolism. Finally, we show that macrophage reprogramming becomes deeply attenuated by 29h. Our findings provide a foundation for understanding macrophage polarization in zebrafish, revealing underpinning molecular mechanisms, including both specific and evolutionarily conserved pathways with a potential impact on translational medicine.

immunology↗