Mme Docteur MATHILDE COUTURIER

Bibliographie

• Methotrexate Restores CD73 Expression on Th1.17 in Rheumatoid Arthritis and Psoriatic Arthritis Patients and May Contribute to Its Anti-Inflammatory Effect through Ado Production

  2019

  ArticleJournal of Clinical Medicine

• Impact of systematic ultrasound of the knee on the rheumatologist’s clinical decision in patients consulting for knee pain

  2016

  ArticleRheumatology International

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Livres & ouvrages

• 📕

  Impact de l’évaluation échographique systématique du genou sur la décision clinique du rhumatologue chez les patients consultant pour une gonalgie

  2014 · 84 p.

Source : Google Books — filtre catégories médicales/santé/sciences.

Localisation

Adresses géocodées via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.

Lieux de consultation

• CH LES ESCARTONS A BRIANCON

  24 Avenue ADRIEN DAURELLE, 05105 Briançon

  ☎ 0492252100Hospitalier🏥 Centre CH ↗🏥 Voir cet établissement

• CABINET DU DR MATHILDE COUTURIER

  28 RUE CENTRALE, 05100 Briançon

  Libéral
  10 m221 m221 m232 m

  © OpenStreetMap · Photos Wikimedia Commons (CC)

  📷 Street View ↗🗺️ Maps ↗OSM ↗

Tarifs & secteur de conventionnement

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

  Pro-Resolving Factors Released by Macrophages After Efferocytosis Promote Mucosal Wound Healing in Inflammatory Bowel Disease

  Frontiers in immunology · 2021

  📚 55 citations🎯 RCR 3.26Top 14% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  Nonresolving inflammation is a critical driver of several chronic inflammatory diseases, including inflammatory bowel diseases (IBD). This unresolved inflammation may result from the persistence of an initiating stimulus or from the alteration of the resolution phase of inflammation. Elimination of apoptotic cells by macrophages (a process called efferocytosis) is a critical step in the resolution phase of inflammation. Efferocytosis participates in macrophage reprogramming and favors the release of numerous pro-resolving factors. These pro-resolving factors exert therapeutic effects in experimental autoimmune arthritis. Here, we propose to evaluate the efficacy of pro-resolving factors produced by macrophages after efferocytosis, a secretome called SuperMApo, in two IBD models, namely dextran sodium sulfate (DSS)-induced and T cell transfer-induced colitis. Reintroducing these pro-resolving factors was sufficient to decrease clinical, endoscopic and histological colitis scores in ongoing naive T cell-transfer-induced colitis and in DSS-induced colitis. Mouse primary fibroblasts isolated from the colon demonstrated enhanced healing properties in the presence of SuperMApo, as attested by their increased migratory, proliferative and contractive properties. This was confirmed by the use of human fibroblasts isolated from patients with IBD. Exposure of an intestinal epithelial cell (IEC) line to these pro-resolving factors increased their proliferative properties and IEC acquired the capacity to capture apoptotic cells. The improvement of wound healing properties induced by SuperMApo was confirmed in vivo in a biopsy forceps-wound colonic mucosa model. Further in vivo analysis in naive T cell transfer-induced colitis model demonstrated an improvement of intestinal barrier permeability after administration of SuperMApo, an intestinal cell proliferation and an increase of α-SMA expression by fibroblasts, as well as a reduction of the transcript coding for fibronectin (Fn1). Finally, we identified TGF-β, IGF-I and VEGF among SuperMApo as necessary to favor mucosal healing and confirmed their role both in vitro (using neutralizing antibodies) and in vivo by depleting these factors from efferocytic macrophage secretome using antibody-coated microbeads. These growth factors only explained some of the beneficial effects induced by factors released by efferocytic macrophages. Overall, the administration of pro-resolving factors released by efferocytic macrophages limits intestinal inflammation and enhance tissue repair, which represents an innovative treatment of IBD.

• 2

  Factors Produced by Macrophages Eliminating Apoptotic Cells Demonstrate Pro-Resolutive Properties and Terminate Ongoing Inflammation

  Frontiers in immunology · 2018

  📚 44 citations🎯 RCR 1.46🔓 Open Access📄 PDF gratuit ↗
• 3

  TGF-beta-exposed plasmacytoid dendritic cells participate in Th17 commitment

  Journal of immunology (Baltimore, Md. : 1950) · 2011

  📚 40 citations🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  Abstract TGF-β is required for both Foxp3+ regulatory T cell (Treg) and Th17 commitment. Plasmacytoid DCs (pDC) have been shown to participate to both Treg and Th17 commitment as well. However, few studies have evaluated the direct effect of TGF-β on pDC, and to our knowledge, no study has assessed the capacity of TGF-β–exposed pDC to polarize naive CD4+ T cells. In this paper, we show that TGF-β–treated pDC favor Th17 but not Treg commitment. This process involves a TGF-β/Smad signal, because TGF-β treatment induced Smad2 phosphorylation in pDC and blockade of TGF-β signaling with the SD208 TGF-βRI kinase inhibitor abrogated Th17 commitment induced by TGF-β–treated pDC. Moreover, TGF-β mRNA synthesis and active TGF-β release were induced in TGF-β–treated pDC and anti–TGF-β Ab blocked Th17 commitment. Unexpectedly, TGF-β treatment also induced increased IL-6 production by pDC, which serves as the other arm for Th17 commitment driven by TGF-β–exposed pDC, because elimination of IL-6–mediated signal with either IL-6– or IL-6Rα–specific Abs prevented Th17 commitment. The in vivo pathogenic role of TGF-β–treated pDC was further confirmed in the Th17-dependent collagen-induced arthritis model in which TGF-β–treated pDC injection significantly increased arthritis severity and pathogenic Th17 cell accumulation in the draining lymph nodes. Thus, our data reveal a previously unrecognized effect of TGF-β–rich environment on pDC ability to trigger Th17 commitment. Such findings have implications in the pathogenesis of autoimmune diseases or immune responses against mucosal extracellular pathogens.

Publications scientifiques (9) — classées par pathologie

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

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