The pathogenesis of anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitides (detected by the indirect immunofluoresecnec of neutrophilsis, upper left panel)) characterized by the involvement of neutrophils as cardinal cells that are activated and responsible for the vessel wall injury resulting in lung and renal lesions (see lower left panel). Neutrophil activation increases expression of granule proteins such as proteinase 3 (PR3) in Wegener’s granulomatosis, that are targeted by specific autoantibodies exerting pathogenic effects. Immune perturbations extend to other target cells such as endothelial cells with potential deleterious effects or macrophages (right panel).
The team has a multidisciplinary and integrative project with three aims:
These projects should provide new insights into the pathophysiology of vasculitis and hopefully help to develop new biomarkers and novative strategies in vascular and/or inflammatory diseases.