Sophie Ohlsson

TL;DR: This study confirms that the pathogenesis of ANCA-associated vasculitis has a genetic component, shows genetic distinctions between granulomatosis with polyang iitis and microscopic polyangiitis that are associated with ANCA specificity, and suggests that the response against the autoantigen proteinase 3 is a central pathogenic feature ofproteinase 3 ANCA -associated vasulitis.

TL;DR: Double-positive patients have a truly hybrid disease phenotype, requiring aggressive early treatment for anti-GBM disease, and careful long-term follow-up and consideration for maintenance immunosuppression for AAV.

TL;DR: A genome-wide association study of EGPA is described that reveals clinical and genetic differences between subgroups stratified by autoantibody status (ANCA), and four candidate genes are targets of therapies in development, supporting their exploration in EGPA.

TL;DR: It is shown that neutrophils are a major source of ficolin‐1, which can be readily exocytosed by stimulation, and the majority becomes associated with the surface membrane of the cells and can be detected by flow cytometry.

TL;DR: It is found that levels of proteinase 3 (PR3), one of the main ANCA antigens, are increased in patients with active disease, regardless of ANCA specificity, and this was not due to decreased renal function, ongoing inflammation or neutrophil activation.