📇 Rhumatologue ·
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Praticien-chercheur
13 articles scientifiques publiés — formation continue solide
✨ Génération du profil synthétique IA en cours…
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Clinical and experimental immunology · 2016
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.
International journal of molecular sciences · 2018
Psoriasis is a chronic systemic inflammatory disease causing erythematosus and scaly skin plaques; up to 30% of patients with psoriasis develop Psoriatic Arthritis (PsA), which is characterised by inflammation and progressive damage of the peripheral joints and/or the spine and/or the entheses. The pathogenic mechanisms driving the skin disorder in psoriasis and the joint disease in PsA are sustained by the activation of inflammatory pathways that can be overlapping, but also, at least partially, distinct. Cytokines members of the IL-23/IL-17 family, critical in the development of autoimmunity, are abundantly expressed within the cutaneous lesions but also seem to be involved in chronic inflammation and damage of the synovium though, as it will be here discussed, not in all patients. In this review, we will focus on the state of the art of the molecular features of psoriatic skin and joints, focusing on the specific role of the IL-23/IL-17 pathway in each of these anatomical districts. We will then offer an overview of the approved and in-development biologics targeting this axis, emphasising how the availability of the “target” in the diseased tissues could provide a plausible explanation for the heterogeneous clinical efficacy of these drugs, thus opening future perspective of personalised therapies.
International journal of molecular sciences · 2019
The interleukin (IL)-1 family of cytokines is composed of 11 members, including the most recently discovered IL-36α, β, γ, IL-37, and IL-38. Similar to IL-1, IL-36 cytokines are initiators and amplifiers of inflammation, whereas both IL-37 and IL-38 display anti-inflammatory activities. A few studies have outlined the role played by these cytokines in several inflammatory diseases. For instance, IL-36 agonists seem to be relevant for the pathogenesis of skin psoriasis whereas, despite being expressed within the synovial tissue, their silencing or overexpression do not critically influence the course of arthritis in mice. In this review, we will focus on the state of the art of the molecular features and biological roles of IL-36, IL-37, and IL-38 in representative skin- and joint-related inflammatory diseases, namely psoriasis, rheumatoid arthritis, and psoriatic arthritis. We will then offer an overview of the therapeutic potential of targeting the IL-36 axis in these diseases, either by blocking the proinflammatory agonists or enhancing the physiologic inhibitory feedback on the inflammation mediated by the antagonists IL-37 and IL-38.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Osteoarthritis and cartilage · 2024 · Journal Article
Boutet MA, Nerviani A, Fossati-Jimack L, Hands-Greenwood R, et al.
Joint bone spine · 2024 · Journal Article
Ghirardi GM, Delrosso CA, Nerviani A, Boutet MA
Drug discovery today · 2024 · Journal Article
Gaigeard N, Cardon A, Le Goff B, Guicheux J, et al.
Osteoarthritis and cartilage · 2022 · Journal Article
Bodic B, Boutet MA, Boyer C, Metayer B, et al.
Joint bone spine · 2021 · Journal Article
Delplace V, Boutet MA, Le Visage C, Maugars Y, et al.
Rheumatology (Oxford, England) · 2020 · Journal Article
Boutet MA, Nerviani A, Lliso-Ribera G, Lucchesi D, et al.
Bone · 2017 · Journal Article
Bougault C, El Jamal A, Briolay A, Mebarek S, et al.
Clinical and experimental immunology · 2016 · Journal Article
Boutet MA, Bart G, Penhoat M, Amiaud J, et al.
Translational research : the journal of laboratory and clinical medicine · 2015 · Journal Article
Bougault C, Briolay A, Boutet MA, Pilet P, et al.
Annals of the rheumatic diseases · 2021 · Journal Article
Nerviani A, Boutet MA, Tan WSG, Goldmann K, et al.
International journal of molecular sciences · 2018 · Journal Article
Boutet MA, Nerviani A, Gallo Afflitto G, Pitzalis C
BMC rheumatology · 2025 · Journal Article
Pattappa G, Karlsson NG, Steinecker-Frohnwieser B, Mobasheri A, et al.
International journal of molecular sciences · 2019 · Journal Article
Boutet MA, Nerviani A, Pitzalis C
International journal of molecular sciences · 2018 · Journal Article
Boutet MA, Nerviani A, Gallo Afflitto G, Pitzalis C
✨ Profil synthétique
IA · 23/05/2026MME Marie-Louise BOUTET est une rhumatologue qui a publié des travaux sur les pathologies traitées par les thérapies anti-IL-23 et anti-IL-17. Ses publications sur PubMed reflètent son intérêt pour ces domaines spécifiques de la rhumatologie. Elle a également contribué à des revues générales dans ce domaine.
Expertises présumées
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.