Docteur Dominique PEROCHEAU

Bibliographie

• eDOL mHealth App and Web Platform for Self-monitoring and Medical Follow-up of Patients With Chronic Pain: Observational Feasibility Study

  2022

  ArticleJMIR Formative Research

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

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Top publications · les plus citées

• 1

  IFN-λ resolves inflammation via suppression of neutrophil infiltration and IL-1β production

  The Journal of experimental medicine · 2015

  📚 188 citations🎯 RCR 5.79Top 6% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  The most studied biological role of type III interferons (IFNs) has so far been their antiviral activity, but their role in autoimmune and inflammatory diseases remains largely unexplored. Here, we show that treatment with IFN-λ2/IL-28A completely halts and reverses the development of collagen-induced arthritis (CIA) and discover cellular and molecular mechanisms of IL-28A antiinflammatory function. We demonstrate that treatment with IL-28A dramatically reduces numbers of proinflammatory IL-17–producing Th17 and γδ T cells in the joints and inguinal lymph nodes, without affecting T cell proliferative responses or levels of anticollagen antibodies. IL-28A exerts its antiinflammatory effect by restricting recruitment of IL-1b–expressing neutrophils, which are important for amplification of inflammation. We identify neutrophils as cells expressing high levels of IFN-λ receptor 1 (IFNLR1)–IL-28 receptor α (IL28RA) and targeted by IL-28A. Our data highlight neutrophils as contributors to the pathogenesis of autoimmune arthritis and present IFN-λs or agonists of IFNLR1–IL28RA as putative new therapeutics for neutrophil-driven inflammation.

• 2

  IRF5 controls both acute and chronic inflammation

  Proceedings of the National Academy of Sciences of the United States of America · 2015

  📚 130 citations🎯 RCR 3.75Top 12% NIH🔓 Open Access

  Lire l'abstract Crossref ↓

  SignificanceMany of the world’s major chronic diseases are driven by inflammation. The most abundant inflammatory cells in these diseases are myeloid cells, such as macrophages and neutrophils. Both cell types show remarkable phenotypic diversity among tissues. Defining molecular factors that control this diversity provides abundant scope for the generation of more specific and effective therapeutics, as the lack of specificity of the current most widely used antiinflammatory approaches, such as glucocorticoids and nonsteroidal antiinflammatory molecules, leads to widespread problems if used long term, even at relatively low doses. In this study we demonstrate that a transcription factor called IFN regulatory factor 5 controls macrophage and neutrophil aspects of inflammation, and thus its blockade might be an effective therapeutic strategy for multiple indications.

• 3

  IRF5 is a specific marker of inflammatory macrophages in vivo

  Mediators of inflammation · 2013

  📚 112 citations🎯 RCR 3.06Top 16% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  Macrophages are an integral part of the innate immune system and key players in pathogen clearance and tissue remodelling. Both functions are accomplished by a pivotal network of different macrophage subtypes, including proinflammatory M1 and anti-inflammatory M2 macrophages. Previously, our laboratory identified the transcription factor interferon regulatory factor 5 (IRF5) as the master regulator of the M1 macrophage polarisation. IRF5 was found to be highly expressed in human M1 compared to M2 macrophages. Furthermore, IRF5 dictates the expression of proinflammatory genes such asIL12bandIL23awhilst repressing anti-inflammatory genes likeIL10. Here we show that murine bone marrow derived macrophages differentiatedin vitrowith GM-CSF are also characterised by high levels of IRF5 mRNA and protein and express proinflammatory cytokines upon LPS stimulation. These macrophages display characteristic expression of M1-marker MHC II but lack the M2-marker CD206. Significantly, we develop intracellular staining of IRF5- expressing macrophages and utilise it to recapitulate thein vitroresults in anin vivomodel of antigen-induced arthritis, emphasising their physiological relevance. Thus, we establish the species-invariant role of IRF5 in controlling the inflammatory macrophage phenotype bothin vitroand inin vivo.

Publications scientifiques (11) — classées par pathologie

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