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Rhumatologue

Docteur JEAN FRANCIS MAILLEFERT

📍 Dijon (21)HospitalierRPPS 10002149572
📊 Reconnaissance scientifique : 32/100📝 147 articles publiés📚 HAL (8)

✨ Profil synthétique

IA · 06/05/2026

Le Docteur Jean Francis Mailléfer est un rhumatologue hospitalier à Dijon, avec une production scientifique significative dans le domaine de la rhumatologie. Ses recherches portent principalement sur les thérapies et les mécanismes des maladies rhumatismales, notamment l'arthrite rhumatoïde, la spondylarthrite et l'ostéoarthrose. Avec un h-index de 32 et 147 publications, il démontre une activité de recherche soutenue.

Expertises présumées

  • Arthrite rhumatoïde
  • Spondylarthrite
  • Ostéoarthrose
  • Goutte
  • Biothérapies non-anti-TNF
  • Pharmacovigilance
  • Prothèse du genou

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.

Activité de recherche & publications

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

h-index

32

h articles cités ≥ h fois chacun. Un h de 32 = 32 publications avec 32+ citations.

Citations

3 435

Publications

147

i10-index

58

Thématiques principales

  • Rheumatoid Arthritis Research and Therapies ×64
  • Spondyloarthritis Studies and Treatments ×32
  • Osteoarthritis Treatment and Mechanisms ×28
  • Total Knee Arthroplasty Outcomes ×21
  • Psoriasis: Treatment and Pathogenesis ×14

Affiliations FR : Inserm · Université de Bourgogne · CHU Dijon Bourgogne

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

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).

Prendre rendez-vous & contact

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
    Brief report: inhibition of interleukin-6 function corrects Th17/Treg cell imbalance in patients with rheumatoid arthritis

    Arthritis and rheumatism · 2012

    📚 287 citations🎯 RCR 7.82Top 4% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    Abstract Objective From an immunologic standpoint, the mechanisms by which treatment with tocilizumab (TCZ), a humanized anti–interleukin‐6 (anti–IL‐6) receptor antibody, results in improvement in rheumatoid arthritis (RA) patients are still not fully understood. In vitro studies and studies in mouse models have demonstrated the critical role of IL‐6 in Th17 cell differentiation. Th17 lymphocytes have been shown to be strongly involved in RA pathogenesis, and the purpose of this study was to investigate the effect of IL‐6 blockade on the balance between Th17 cells and Treg cells in patients with active RA. Methods Patients with active RA for whom TCZ had been prescribed by a rheumatologist were enrolled in this study. Phenotypic analyses of T cell populations were performed, and the Disease Activity Score in 28 joints (DAS28) was assessed. Serum cytokine levels and other parameters of inflammation were measured before the first infusion and after the third infusion of TCZ (8 mg/kg). Results Compared to controls, levels of Th17 cells (CD4+IL‐17+) were increased and Treg cells (CD4+CD25 high FoxP3+) were decreased in the peripheral blood of patients with active RA. The suppressive function of circulating Treg cells was not impaired in patients with active RA. TCZ treatment induced a significant decrease in the DAS28 associated with a significant decrease in the percentage of Th17 cells (from a median of 0.9% to 0.45%; P = 0.009) and an increase in the percentage of Treg cells (from a median of 3.05% to 3.94%; P = 0.0039) in all patients. Conclusion This study demonstrates for the first time that inhibition of IL‐6 function by TCZ corrects the imbalance between Th17 cells and Treg cells in patients with RA.

  • 2
    Th1 and Th17 lymphocytes expressing CD161 are implicated in giant cell arteritis and polymyalgia rheumatica pathogenesis

    Arthritis and rheumatism · 2012

    📚 167 citations🎯 RCR 4.80Top 8% NIH
    Lire l'abstract Crossref ↓

    AbstractObjectiveGiant cell arteritis (GCA) is the most frequently occurring vasculitis in elderly individuals, and its pathogenesis is not fully understood. The objective of this study was to decipher the role of the major CD4+ T cell subsets in GCA and its rheumatologic form, polymyalgia rheumatica (PMR).MethodsA prospective study of the phenotype and the function of major CD4+ T cell subsets (Th1, Th17, and Treg cells) was performed in 34 untreated patients with GCA or PMR, in comparison with 31 healthy control subjects and with the 27 treated patients who remained after the 7 others withdrew.ResultsCompared with control subjects, patients with GCA and patients with PMR had a decreased frequency of Treg cells and Th1 cells, whereas the percentage of Th17 cells was significantly increased. Furthermore, an analysis of temporal artery biopsy specimens obtained from patients affected by GCA for whom biopsy results were positive demonstrated massive infiltration by Th17 and Th1 lymphocytes without any Treg cells. After glucocorticoid treatment, the percentages of circulating Th1 and Th17 cells decreased, whereas no change in the Treg cell frequency was observed. The frequency of CD161+CD4+ T cells, which are considered to be Th17 cell precursors, was similar in patients and control subjects. However, these cells highly infiltrated GCA temporal artery biopsy specimens, and their ability to produce interleukin‐17 in vitro was significantly enhanced in patients with GCA and patients with PMR and was correlated with a decrease in the phosphorylated form of STAT‐1.ConclusionThis study is the first to demonstrate that the frequency of Treg cells is decreased in patients with GCA and patients with PMR, and that CD161+CD4+ T lymphocytes, differentiated into Th1 cells and Th17 cells, are involved in the pathogenesis of GCA and PMR.

Publications scientifiques (50) — classées par pathologie

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

Transversal32

Biothérapies non-anti-TNF8

Goutte3

Pharmacovigilance3

Vraie vie / RWE3

Revue / méta-analyse2

Revue générale2

Arthrose1

Essai clinique1

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