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Rhumatologue

Professeur JEAN SIBILIA

📍 Strasbourg (67)HospitalierRPPS 10002430105
📊 Reconnaissance scientifique : 94/100📝 950 articles publiés📚 HAL (8)📕 6 livres🎓 6 thèses dirigées

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🎓 Diplômes

  • DE Docteur en médecine

Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.

Thèses universitaires

Source : catalogue national des thèses theses.fr (ABES). Ne couvre que les doctorats / HDR — les thèses d'exercice (DES) sont archivées dans les SCD universitaires.

Direction de thèses

🎓 6 thèses dirigées

Source theses.fr — signal de direction d'équipe / statut PU-PH (à confirmer via le site universitaire).

Activité de recherche & publications

Source : bases de données publiques (OpenAlex, PubMed).

h-index

94

h articles cités ≥ h fois chacun. Un h de 94 = 94 publications avec 94+ citations.

Citations

32 325

Publications

950

i10-index

407

Thématiques principales

  • Rheumatoid Arthritis Research and Therapies ×248
  • Systemic Lupus Erythematosus Research ×190
  • Systemic Sclerosis and Related Diseases ×128
  • Inflammatory Myopathies and Dermatomyositis ×94
  • Spondyloarthritis Studies and Treatments ×91

Affiliations FR : Immunologie, Immunopathologie et Chimie Thérapeutique · Université de Strasbourg

Voir sur OpenAlex ↗🆔 ORCID 0000-0002-1601-4795

Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.

Bibliographie

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Livres & ouvrages

Source : Google Books — filtre catégories médicales/santé/sciences.

Localisation des cabinets

Adresses géocodées via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.

Lieux de consultation

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

📊 Comprendre le remboursement

Prendre rendez-vous & contact

🗓 Trouver sur Doctolib📇 Ajouter à mes contacts

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Articles de presse (9)

Source : Google News (recherche par nom complet — homonymes possibles, vérifier le contenu).

Top publications · les plus citées

  • 1
    Identification of driver genes for critical forms of COVID-19 in a deeply phenotyped young patient cohort

    Science translational medicine · 2022

    📚 98 citations🎯 RCR 6.55Top 5% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    The drivers of critical coronavirus disease 2019 (COVID-19) remain unknown. Given major confounding factors such as age and comorbidities, true mediators of this condition have remained elusive. We used a multi-omics analysis combined with artificial intelligence in a young patient cohort where major comorbidities were excluded at the onset. The cohort included 47 “critical” (in the intensive care unit under mechanical ventilation) and 25 “non-critical” (in a non-critical care ward) patients with COVID-19 and 22 healthy individuals. The analyses included whole-genome sequencing, whole-blood RNA sequencing, plasma and blood mononuclear cell proteomics, cytokine profiling, and high-throughput immunophenotyping. An ensemble of machine learning, deep learning, quantum annealing, and structural causal modeling were used. Patients with critical COVID-19 were characterized by exacerbated inflammation, perturbed lymphoid and myeloid compartments, increased coagulation, and viral cell biology. Among differentially expressed genes, we observed up-regulation of the metalloprotease ADAM9 . This gene signature was validated in a second independent cohort of 81 critical and 73 recovered patients with COVID-19 and was further confirmed at the transcriptional and protein level and by proteolytic activity. Ex vivo ADAM9 inhibition decreased severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uptake and replication in human lung epithelial cells. In conclusion, within a young, otherwise healthy, cohort of individuals with COVID-19, we provide the landscape of biological perturbations in vivo where a unique gene signature differentiated critical from non-critical patients. We further identified ADAM9 as a driver of disease severity and a candidate therapeutic target.

  • 2
    A Risk Score to Detect Subclinical Rheumatoid Arthritis-Associated Interstitial Lung Disease

    Arthritis & rheumatology (Hoboken, N.J.) · 2022

    📚 83 citations🎯 RCR 9.25Top 3% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    ObjectivePatients at high risk of rheumatoid arthritis–associated interstitial lung disease (RA‐ILD) would benefit from being identified before the onset of respiratory symptoms; this can be done by screening patients with the use of chest high‐resolution computed tomography (HRCT). Our objective was to develop and validate a risk score for patients who have subclinical RA‐ILD.MethodsOur study included a discovery population and a replication population from 2 prospective RA cohorts (ESPOIR and TRANSLATE2, respectively) without pulmonary symptoms who had received chest HRCT scans. All patients were genotyped for MUC5B rs35705950. After multiple logistic regression, a risk score based on independent risk factors for subclinical RA‐ILD was developed in the discovery population and tested for validation in the replication population.ResultsThe discovery population included 163 patients with RA, and the replication population included 89 patients with RA. The prevalence of subclinical RA‐ILD was 19.0% and 16.9%, respectively. In the discovery population, independent risk factors for subclinical RA‐ILD were presence of the MUC5B rs35705950 T allele (odds ratio [OR] 3.74 [95% confidence interval (95% CI) 1.37, 10.39]), male sex (OR 3.93 [95% CI 1.40, 11.39]), older age at RA onset (for each year, OR 1.10 [95% CI 1.04, 1.16]), and increased mean Disease Activity Score in 28 joints using the erythrocyte sedimentation rate (for each unit, OR 2.03 [95% CI 1.24, 3.42]). We developed and validated a derived risk score with receiver operating characteristic areas under the curve of 0.82 (95% CI 0.70–0.94) for the discovery population and 0.78 (95% CI 0.65–0.92) for the replication population. Excluding MUC5B rs35705950 from the model provided a lower goodness of fit (likelihood ratio test, P = 0.01).ConclusionWe developed and validated a risk score that could help identify patients at high risk of subclinical RA‐ILD. Our findings support an important contribution of MUC5B rs35705950 to subclinical RA‐ILD risk.

  • 3
    Variability of Primary Sjögren's Syndrome Is Driven by Interferon-α and Interferon-α Blood Levels Are Associated With the Class II HLA-DQ Locus

    Arthritis & rheumatology (Hoboken, N.J.) · 2022

    📚 42 citations🎯 RCR 3.82Top 12% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    ObjectivePrimary Sjögren's syndrome (SS) is the second most frequent systemic autoimmune disease, affecting 0.1% of the general population. To characterize the molecular and clinical variabilities among patients with primary SS, we integrated transcriptomic, proteomic, cellular, and genetic data with clinical phenotypes in a cohort of 351 patients with primary SS.MethodsWe analyzed blood transcriptomes and genotypes of 351 patients with primary SS who were participants in a multicenter prospective clinical cohort. We replicated the transcriptome analysis in 3 independent cohorts (n = 462 patients). We determined circulating interferon‐α (IFNα) and IFNγ protein concentrations using digital single molecular arrays (Simoa).ResultsTranscriptome analysis of the prospective cohort showed a strong IFN gene signature in more than half of the patients; this finding was replicated in the 3 independent cohorts. Because gene expression analysis did not discriminate between type I IFN and type II IFN, we used Simoa to demonstrate that the IFN transcriptomic signature was driven by circulating IFNα and not by IFNγ protein levels. IFNα protein levels, detectable in 75% of patients, were significantly associated with clinical and immunologic features of primary SS disease activity at enrollment and with increased frequency of systemic complications over the 5‐year follow‐up. Genetic analysis revealed a significant association between IFNα protein levels, a major histocompatibility (MHC) class II haplotype, and anti‐SSA antibody. Additional cellular analysis revealed that an MHC class II HLA–DQ locus acts through up‐regulation of HLA class II molecules on conventional dendritic cells.ConclusionWe identified the predominance of IFNα as a driver of primary SS variability, with IFNα demonstrating an association with HLA gene polymorphisms.

Publications scientifiques (50) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

Transversal23

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Lupus6

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Sjögren5

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Épidémiologie & registres3

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Biothérapies non-anti-TNF2

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Case report / série2

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csDMARDs2

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Pharmacovigilance2

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Anti-TNF1

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Microbiote1

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Revue / méta-analyse1

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Revue générale1

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Rhumatisme psoriasique1

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Santé mentale / fatigue1

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Vascularites des gros vaisseaux1

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Datasets & protocoles partagés

Source : DataCite — DOIs pour datasets, logiciels, protocoles, registres patient. Hors articles (déjà couverts).

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