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Rhumatologue

Docteur BENOIT LE GOFF

📍 Nantes (44)HospitalierRPPS 10004041165
📊 Reconnaissance scientifique : 38/100📝 382 articles publiés📚 HAL (8)🎓 5 thèses dirigées

✨ Profil synthétique

IA · 29/04/2026

Le Docteur BENOIT LE GOFF est un rhumatologue hospitalier à Nantes, avec une production scientifique importante (h-index de 38 et 382 publications). Ses recherches portent principalement sur les maladies rhumatismales, notamment la polyarthrite rhumatoïde et les spondylarthropathies. Il a également dirigé plusieurs thèses de doctorat dans le domaine de l'immunologie et de la biologie moléculaire.

Expertises présumées

  • Polyarthrite rhumatoïde
  • Spondylarthropathies
  • Tendinopathies
  • Biothérapies
  • Thérapies anti-TNF
  • csDMARDs
  • Pathologies de la synoviale

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

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

🎓 5 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

38

h articles cités ≥ h fois chacun. Un h de 38 = 38 publications avec 38+ citations.

Citations

4 999

Publications

382

i10-index

104

Thématiques principales

  • Rheumatoid Arthritis Research and Therapies ×81
  • Spondyloarthritis Studies and Treatments ×65
  • Shoulder Injury and Treatment ×49
  • Orthopedic Infections and Treatments ×40
  • Musculoskeletal synovial abnormalities and treatments ×38

Affiliations FR : Inserm · Oniris · Nantes Université

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).

Lieu de consultation

Tarifs & secteur de conventionnement

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

Prendre rendez-vous & contact

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

Vidéos & interventions (12)

Source YouTube · recherche par nom (homonymes possibles).

Top publications · les plus citées

  • 1
    Novel insights into macrophage diversity in rheumatoid arthritis synovium

    Autoimmunity reviews · 2021

    📚 120 citations🎯 RCR 8.17Top 4% NIH🔓 Open Access
  • 2
    MicroRNA-17-5p Reduces Inflammation and Bone Erosions in Mice With Collagen-Induced Arthritis and Directly Targets the JAK/STAT Pathway in Rheumatoid Arthritis Fibroblast-like Synoviocytes

    Arthritis & rheumatology (Hoboken, N.J.) · 2020

    📚 90 citations🎯 RCR 4.97Top 8% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    ObjectiveWe undertook this study to examine microRNA (miRNA) expression across rheumatoid arthritis (RA) phenotypes, along with the effects and mechanisms of action of miRNA‐17‐5p (miR‐17).MethodsA miRNA array was performed in synovial tissue biopsied from patients with naive erosive RA (n = 3) and patients with nonerosive RA (n = 3). MicroRNA‐17 lipoplex was delivered intraarticularly in the murine collagen‐induced arthritis model. Clinical, histologic, and structural effects were studied over the course of arthritis. In‐depth studies of the mechanisms of action of miR‐17 were performed in primary RA fibroblast‐like synoviocytes (FLS) isolated from synovial tissue.ResultsFifty‐five miRNAs including miR‐17 were reduced in erosive RA. The miR‐17 transfection into arthritic paws reduced the clinical inflammation score between day 2 and day 7 (2.8 versus 1.9; P = 0.03). Synovial B cell, T cell, macrophage, and polynuclear neutrophil infiltration was significantly reduced. Structural damage was also decreased, as shown by a reduction in the number of osteoclasts detected using tartrate‐resistant acid phosphatase staining (osteoclast surface/bone surface 32% versus 18%; P = 0.005) and erosion score by computed tomography analysis (2.9 versus 1.7; P = 0.023). Proinflammatory cytokines from the interleukin‐6 (IL‐6) family and IL‐1β expression were also significantly reduced, but tumor necrosis factor was not. MicroRNA‐17 directly targeted the 3′‐untranslated regions of STAT3 and JAK1. STAT3 and JAK1 messenger RNA (mRNA) and protein expression were reduced in RA FLS following miR‐17 transfection. STAT3 and JAK1 mRNA and activation of STAT3, as assessed by immunohistochemistry, were also reduced in injected paws (% stained area 93% versus 62%; P = 0.035).ConclusionWe demonstrate an antiinflammatory and antierosive role of miR‐17 in vivo. This effect involves the suppression of the IL‐6 family autocrine‐amplifying loop through the direct targeting of JAK1 and STAT3.

  • 3
    Methotrexate effect on immunogenicity and long-term maintenance of adalimumab in axial spondyloarthritis: a multicentric randomised trial

    RMD open · 2020

    📚 46 citations🎯 RCR 3.11Top 15% NIH🩺 Clinique🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    Objectives Anti-drug antibodies (ADA) are responsible for decreased adalimumab efficacy in axial spondyloarthritis (SpA). We aimed to evaluate the ability of methotrexate (MTX) to decrease adalimumab immunisation. Methods A total of 110 patients eligible to receive adalimumab 40 mg subcutaneously (s.c.) every other week were randomised (1:1 ratio) to receive, 2 weeks before adalimumab (W-2) and weekly, MTX 10 mg s.c. (MTX+) or not (MTX−). ADA detection and adalimumab serum concentration were assessed at weeks 4 (W4), 8 (W8), 12 (W12) and 26 (W26) after starting adalimumab (W0). The primary outcome was the proportion of patients with ADA at W26. Four years after the study completion, we retrospectively analysed adalimumab maintenance in relation with MTX co-treatment duration. Results We analysed data for 107 patients (MTX+; n=52; MTX-; n=55). ADA were detected at W26 in 39/107 (36.4%) patients: 13/52 (25%) in the MTX+ group and 26/55 (47.3%) in the MTX− group (p=0.03). Adalimumab concentration was significantly higher in the MTX+ than MTX− group at W4, W8, W12 and W26. The two groups did not differ in adverse events or efficacy. In the follow-up study, MTX co-treatment >W26 versus no MTX or ≤W26 was significantly associated with adalimumab long-term maintenance (p=0.04). Conclusion MTX reduces the immunogenicity and ameliorate the pharmacokinetics of adalimumab in axial SpA. A prolonged co-treatment of MTX>W26 seems to increase adalimumab long-term maintenance.

Publications scientifiques (50) — classées par pathologie

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

Transversal37

Tendinopathies & SCC4

Revue générale3

Anti-TNF2

Biothérapies non-anti-TNF1

Case report / série1

csDMARDs1

Épidémiologie & registres1

Microbiote1

Ostéoporose1

Vraie vie / RWE1

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