📇 Rhumatologue · VANNES · (56) · Libéral

M FRANCK MOREL

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4 raisons identifiées

Encadrant universitaire
Forme la prochaine génération de rhumatologues (3 thèses dirigées)
Praticien-chercheur
11 articles scientifiques publiés — formation continue solide
Expérience confirmée
32 ans d'exercice en rhumatologie — recul clinique solide
Délais de RDV courts dans la région
141.3 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 VANNES (56)LibéralRPPS 10002671567

EnseignementExpérience confirmée

32ans d'exercice (thèse 1994)

📊 Reconnaissance scientifique : 48/100📝 384 articles publiés🇫🇷 Publications académiques françaises (8)🎓 3 thèses dirigées

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.

Top publications · les plus citées

Distinct expression of interleukin (IL)-36α, β and γ, their antagonist IL-36Ra and IL-38 in psoriasis, rheumatoid arthritis and Crohn's disease

Clinical and experimental immunology · 2016

📚 236 citations🎯 RCR 8.77Top 3% NIH🔓 Open Access

Lire l'abstract Crossref ↓

Summary Interleukin (IL)-36α, IL-36β and IL-36γ are expressed highly in skin and are involved in the pathogenesis of psoriasis, while the antagonists IL-36Ra or IL-38, another potential IL-36 inhibitor, limit uncontrolled inflammation. The expression and role of IL-36 cytokines in rheumatoid arthritis (RA) and Crohn's disease (CD) is currently debated. Here, we observed that during imiquimod-induced mouse skin inflammation and in human psoriasis, expression of IL-36α, γ and IL-36Ra, but not IL-36β and IL-38 mRNA, was induced and correlated with IL-1β and T helper type 17 (Th17) cytokines (IL-17A, IL-22, IL-23, CCL20). In mice with collagen-induced arthritis and in the synovium of patients with RA, IL-36α, β, γ, IL-36Ra and IL-38 were all elevated and correlated with IL-1β, CCL3, CCL4 and macrophage colony-stimulating factor (M-CSF), but not with Th17 cytokines. In the colon of mice with dextran sulphate sodium-induced colitis and in patients with CD, only IL-36α, γ and IL-38 were induced at relatively low levels and correlated with IL-1β and IL-17A. We suggest that only a minor subgroup of patients with RA (17–29%) or CD (25%) had an elevated IL-36 agonists/antagonists ratio, versus 93% of patients with psoriasis. By immunohistochemistry, IL-36 cytokines were produced by various cell types in skin, synovium and colonic mucosa such as keratinocytes, CD68+ macrophages, dendritic/Langerhans cells and CD79α+ plasma cells. In primary cultures of monocytes or inflammatory macrophages (M1), IL-36β and IL-36Ra were produced constitutively, but IL-36α, γ and IL-38 were produced after lipopolysaccharide stimulation. These distinct expression profiles may help to explain why only subgroups of RA and CD patients have a potentially elevated IL-36 agonists/antagonists ratio.

Synovial fluid proteomic fingerprint: S100A8, S100A9 and S100A12 proteins discriminate rheumatoid arthritis from other inflammatory joint diseases

Rheumatology (Oxford, England) · 2010

📚 98 citations🎯 RCR 2.66Top 19% NIH

Apolipoprotein A-I and platelet factor 4 are biomarkers for infliximab response in rheumatoid arthritis

Annals of the rheumatic diseases · 2009

📚 66 citations🎯 RCR 1.88🔓 Open Access

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M FRANCK MOREL

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Thèses universitaires

Direction de thèses

Activité de recherche & publications

Publications académiques en France

Lieu de consultation

Tarifs & secteur de conventionnement

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Top publications · les plus citées

Publications scientifiques (11) — classées par pathologie

Transversal8

Anti-IL-171

Anti-TNF1

Pédiatrie1

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