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Biomedical subjects

Brigitte Bader-Meunier

Publications and source records attributed to Brigitte Bader-Meunier.

2 recordsLinked to original sources

Interferon-driven gene signature identifies two distinct subgroups in rheumatoid factor-positive polyarticular juvenile idiopathic arthritis.

OBJECTIVE: To characterize the demographic, clinical, serological, genetic background, course and value of the interferon (IFN)-score in a cohort of patients with rheumatoid factor (RF)-positive polyarticular juvenile idiopathic arthritis (pJIA). METHODS: Monocentric retrospective study of patients with RF-positive pJIA. Demographic, clinical and laboratory data were collected. The IFN-score was calculated based on the expression levels of 24 IFN stimulated genes. Whole exome sequencing was performed in 22 patients. RESULTS: Thirty-two patients were included. The IFN score was positive in 18 patients (56.2%) and negative in 14 patients (43.7%). An increased IFN score was associated with a significantly higher family history of autoimmunity (p = 0.0004), parental first-degree consanguinity (p = 0.05) and prevalence of antibodies to anti-cyclic citrullinated peptide (ACPA) (p = 0.01). Three patients with interstitial lung disease exhibited a positive IFN score. Conversely, demographic features and characteristics of polyarthritis did not differ between the two groups. Clinically inactive disease was achieved in 21/32 (66%) patients, with no significant difference according to the IFN score. Remission was never achieved with methotrexate alone. We identified one patient with a pathogenic de novo mutation in COPA. Additionally, ultra-rare variants in genes related to IFN and/or innate immunity were found in 21/22 (95.5%) patients. CONCLUSION: The IFN signature identified two distinct subgroups in RF-positive pJIA according to family history and immunological features. Our study suggests that patients with an elevated IFN score should be screened for pulmonary involvement. Future prospective studies are required to validate the use of the IFN score as a biomarker in RF-positive pJIA.

Rheumatoid factor

NAP1 switches from an activator to a limiter of interferon induction by trapping TBK1 in condensates.

TBK1 kinase is a central regulator of type I IFN production. Upon activation of the IFN-β induction pathway, TBK1-adaptor proteins (NAP1, SINTBAD, TANK) form liquid condensates. We show that NAP1 condensates concentrate TBK1. Using NAP1KO cell lines, we demonstrate that NAP1 exerts a dual effect on TBK1 activity. Initially, NAP1 binds TBK1 and increases its activity, promoting IFN pathway activation. Subsequently, TBK1-mediated phosphorylation of NAP1 induces the formation of condensates. These NAP1 condensates concentrate both TBK1 and the phosphatase PP2A, which dephosphorylates and consequently deactivates TBK1, thus limiting IFN induction. Additionally, in patients with lupus or interferonopathies, we identify NAP1 variants unable to form condensates upon danger signal exposure, which sustain TBK1 activation without limiting its activity. This study reveals a mode of regulating a signaling pathway through condensate formation and provides a potential molecular explanation for immune dysregulation associated with NAP1 variants in certain patients with interferonopathies.

Protein Serine-Threonine Kinases