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Rhumatologue

Docteur FABIENNE COURY

📍 Oullins-Pierre-Bénite (69)HospitalierRPPS 10003133807
📊 Reconnaissance scientifique : 21/100📝 132 articles publiés📚 HAL (8)

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🎓 Diplômes

  • DE Docteur en médecine

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

Activité de recherche & publications

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

h-index

21

h articles cités ≥ h fois chacun. Un h de 21 = 21 publications avec 21+ citations.

Citations

1 910

Publications

132

i10-index

32

Thématiques principales

  • Rheumatoid Arthritis Research and Therapies ×43
  • Autoimmune and Inflammatory Disorders Research ×21
  • Spondyloarthritis Studies and Treatments ×20
  • Bone Metabolism and Diseases ×13
  • Inflammatory Myopathies and Dermatomyositis ×11

Affiliations FR : Université Claude Bernard Lyon 1 · Inserm · Centre de Recherche en Neurosciences de Lyon

Voir sur OpenAlex ↗🆔 ORCID 0000-0002-9175-8620

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).

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).

Top publications · les plus citées

  • 1
    Langerhans cell histiocytosis reveals a new IL-17A-dependent pathway of dendritic cell fusion

    Nature medicine · 2008

    📚 154 citations🎯 RCR 3.42Top 13% NIH
  • 2
    Infliximab therapy in rheumatoid arthritis and ankylosing spondylitis-induced specific antinuclear and antiphospholipid autoantibodies without autoimmune clinical manifestations: a two-year prospective study

    Arthritis research & therapy · 2004

    📚 97 citations🎯 RCR 2.77Top 18% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    AbstractTreatment of rheumatoid arthritis (RA) with infliximab (Remicade®) has been associated with the induction of antinuclear autoantibodies (ANA) and anti-double-stranded DNA (anti-dsDNA) autoantibodies. In the present study we investigated the humoral immune response induced by infliximab against organ-specific or non-organ-specific antigens not only in RA patients but also in patients with ankylosing spondylitis (AS) during a two-year followup. The association between the presence of autoantibodies and clinical manifestations was then examined. The occurrence of the various autoantibodies was analyzed in 24 RA and 15 AS patients all treated with infliximab and in 30 RA patients receiving methotrexate but not infliximab, using the appropriate methods of detection. Infliximab led to a significant induction of ANA and anti-dsDNA autoantibodies in 86.7% and 57% of RA patients and in 85% and 31% of AS patients, respectively. The incidence of antiphospholipid (aPL) autoantibodies was significantly higher in both RA patients (21%) and AS patients (27%) than in the control group. Most anti-dsDNA and aPL autoantibodies were of IgM isotype and were not associated with infusion side effects, lupus-like manifestations or infectious disease. No other autoantibodies were shown to be induced by the treatment. Our results confirmed the occurrence of ANA and anti-dsDNA autoantibodies and demonstrated that the induction of ANA, anti-dsDNA and aPL autoantibodies is related to infliximab treatment in both RA and AS, with no significant relationship to clinical manifestations.

  • 3
    Murine dendritic cell transdifferentiation into osteoclasts is differentially regulated by innate and adaptive cytokines

    European journal of immunology · 2007

    📚 86 citations🎯 RCR 1.89🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    AbstractDendritic cells (DC) are the mononuclear cells that initiate adaptive immune responses. Osteoclasts (OC) are the multinucleated giant cells that resorb bone. As previously described for human conventional DC (cDC), we demonstrate that murine cDC, either in vitro generated from Fms‐like tyrosine kinase 3 (Flt3)+ bone marrow progenitors or ex vivo purified from spleen, are able to develop into OC in response to M‐CSF and receptor activator of NF‐κB ligand (RANKL) in vitro. This transdifferentiation is driven by the immune environment that controls cDC maturation, cell fusion, tartrate‐resistant acid phosphatase (TRAP) and bone resorption activities. Only immature cDC have the capacity to become OC since mature cDC or plasmacytoid DC do not. Additions of the pro‐inflammatory cytokines, such as IL‐1β and TNF‐α, or human rheumatoid synovial fluid, increase murine cDC transdifferentiation into OC, whereas IFN‐α inhibits it. The adaptive cytokine, IFN‐γ, inhibits cDC fusion while IL‐4 increases it. IL‐2, IFN‐γ and IL‐4 inhibit TRAP and bone resorption activities contrary to IL‐10, which enhances both activities. A putative new “immune multinucleated giant cell” unable to resorb bone, which is formed owing to IL‐4, is underlined. The future analysis of cDC transdifferentiation into OC in murine models of inflammatory arthritis will give us the quantitative importance of this phenomenon in vivo.

Publications scientifiques (50) — classées par pathologie

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

Transversal28

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Anti-TNF8

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Épidémiologie & registres5

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Revue / méta-analyse3

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Biothérapies non-anti-TNF2

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csDMARDs2

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Essai clinique2

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Arthrite juvénile1

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Génétique1

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Ostéoporose1

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Pharmacovigilance1

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Revue générale1

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SAPL1

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Datasets & protocoles partagés

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

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