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Rhumatologue

Docteur SYLVIE SCHMIDT

📍 Bois-Guillaume (76)LibéralRPPS 10001359610
📊 Reconnaissance scientifique : 16/100📝 64 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

16

h articles cités ≥ h fois chacun. Un h de 16 = 16 publications avec 16+ citations.

Citations

939

Publications

64

i10-index

24

Thématiques principales

  • HIV Research and Treatment ×32
  • HIV/AIDS drug development and treatment ×16
  • Immunotherapy and Immune Responses ×14
  • Monoclonal and Polyclonal Antibodies Research ×14
  • Immune Cell Function and Interaction ×14
Voir sur OpenAlex ↗🆔 ORCID 0000-0002-2114-7541

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.

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).

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Prendre rendez-vous & contact

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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
    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
    UNC93B1 variants underlie TLR7-dependent autoimmunity

    Science immunology · 2024

    📚 59 citations🎯 RCR 10.21Top 2% NIH
    Lire l'abstract Crossref ↓

    UNC93B1 is critical for trafficking and function of nucleic acid–sensing Toll-like receptors (TLRs) TLR3, TLR7, TLR8, and TLR9, which are essential for antiviral immunity. Overactive TLR7 signaling induced by recognition of self–nucleic acids has been implicated in systemic lupus erythematosus (SLE). Here, we report UNC93B1 variants (E92G and R336L) in four patients with early-onset SLE. Patient cells or mouse macrophages carrying the UNC93B1 variants produced high amounts of TNF-α and IL-6 and upon stimulation with TLR7/TLR8 agonist, but not with TLR3 or TLR9 agonists. E92G causes UNC93B1 protein instability and reduced interaction with TLR7, leading to selective TLR7 hyperactivation with constitutive type I IFN signaling. Thus, UNC93B1 regulates TLR subtype–specific mechanisms of ligand recognition. Our findings establish a pivotal role for UNC93B1 in TLR7-dependent autoimmunity and highlight the therapeutic potential of targeting TLR7 in SLE.

  • 3
    Galectin-8 induces functional disease markers in human osteoarthritis and cooperates with galectins-1 and -3

    Cellular and molecular life sciences : CMLS · 2018

    📚 49 citations🎯 RCR 2.24Top 23% NIH🔓 Open Access📄 PDF gratuit ↗

Publications scientifiques (50) — classées par pathologie

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

Transversal38

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Case report / série2

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Essai clinique2

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Goutte2

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Activité physique / Rééducation1

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csDMARDs1

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Génétique1

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IA en rhumatologie1

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Lombalgie1

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Lupus1

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Revue / méta-analyse1

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Revue générale1

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Vascularites1

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