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Rhumatologue

Docteur MATHILDE BENHAMOU

📍 Paris 14e Arrondissement (75)MixteRPPS 10005188981
📊 Reconnaissance scientifique : 11/100📝 27 articles publiés📚 HAL (7)

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

11

h articles cités ≥ h fois chacun. Un h de 11 = 11 publications avec 11+ citations.

Citations

690

Publications

27

i10-index

11

Thématiques principales

  • Rheumatoid Arthritis Research and Therapies ×11
  • Spondyloarthritis Studies and Treatments ×8
  • Musculoskeletal Disorders and Rehabilitation ×6
  • Osteoarthritis Treatment and Mechanisms ×3
  • Total Knee Arthroplasty Outcomes ×3

Affiliations FR : Centre Hospitalier Intercommunal de Poissy

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

  • GHU APHP CUP SITE COCHIN PORT ROYAL

    27 Rue DU FAUBOURG SAINT JACQUES, 75679 Paris 14e Arrondissement

    0158414141Hospitalier
  • CABINET DU DR MATHILDE BENHAMOU

    14 BOULEVARD DE LA REPUBLIQUE, 78000 Versailles

    Libéral
  • HOPITAL LA PORTE VERTE

    6 Avenue FRANCHET D ESPEREY, 78004 Versailles

    0139637400Hospitalier

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
    Understanding Fc Receptor Involvement in Inflammatory Diseases: From Mechanisms to New Therapeutic Tools

    Frontiers in immunology · 2019

    📚 228 citations🎯 RCR 9.58Top 3% NIH🔓 Open Access📄 PDF gratuit ↗
  • 2
    Lyn and Fyn function as molecular switches that control immunoreceptors to direct homeostasis or inflammation

    Nature communications · 2017

    📚 97 citations🎯 RCR 3.16Top 15% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    AbstractImmunoreceptors can transduce either inhibitory or activatory signals depending on ligand avidity and phosphorylation status, which is modulated by the protein kinases Lyn and Fyn. Here we show that Lyn and Fyn control immune receptor signaling status. SHP-1 tyrosine 536 phosphorylation by Lyn activates the phosphatase promoting inhibitory signaling through the immunoreceptor. By contrast, Fyn-dependent phosphorylation of SHP-1 serine 591 inactivates the phosphatase, enabling activatory immunoreceptor signaling. These SHP-1 signatures are relevant in vivo, as Lyn deficiency exacerbates nephritis and arthritis in mice, whereas Fyn deficiency is protective. Similarly, Fyn-activating signature is detected in patients with lupus nephritis, underlining the importance of this Lyn–Fyn balance. These data show how receptors discriminate negative from positive signals that respectively result in homeostatic or inflammatory conditions.

  • 3
    Proteinase 3, the Wegener autoantigen, is externalized during neutrophil apoptosis: evidence for a functional association with phospholipid scramblase 1 and interference with macrophage phagocytosis

    Blood · 2007

    📚 96 citations🎯 RCR 2.16Top 24% NIH
    Lire l'abstract Crossref ↓

    AbstractProteinase 3 (PR3), a serine proteinase contained in neutrophil azurophilic granules, is considered a risk factor for vasculitides and rheumatoid arthritis when expressed on the outer leaflet of neutrophil plasma membrane and is the preferred target of antineutrophil cytoplasm autoantibodies (ANCA) in Wegener granulomatosis. ANCA binding to PR3 expressed at the surface of neutrophils activates them. Evidence is provided that neutrophil apoptosis induced significantly more membrane PR3 expression without degranulation (but no enhanced membrane CD35, CD66b, CD63, myeloperoxidase, or elastase expression). This observation was confirmed on cytoplasts, a model of granule-free neutrophils. We hypothesized that PR3 could interact with proteins involved in membrane flip-flop (eg, phospholipid scramblase 1 [PLSCR1]). PR3-PLSCR1 interaction in neutrophils was demonstrated by confocal microscopy and coimmunoprecipitation. In the RBL-2H3 rat mast-cell line stably transfected with PR3 or its inactive mutant (PR3S203A), PR3 externalization depended on PLSCR1, as shown by less PR3 externalization in the presence of rPLSCR1 siRNA, but independently of its serine-proteinase activity. Finally, apoptosis-externalized PR3 decreased the human macrophage-phagocytosis rate of apoptotic PR3 transfectants. Therefore, in addition to ANCA binding in vasculitis, the proinflammatory role of membrane PR3 expression may involve interference with macrophage clearance of apoptotic neutrophils.

Publications scientifiques (24) — classées par pathologie

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

Transversal20

Anti-TNF1

Case report / série1

Connectivite mixte1

Vascularites1

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