Docteur Léa PERROT

Bibliographie

• Novel CNNM2 variant causing hypomagnesemia and early-onset calcium pyrophosphate deposition disease: A case report

  2026

  ArticleJoint Bone Spine

• Spondylodiscitis revealing Whipple disease

  2025

  ArticleSkeletal Radiology

• Factors associated with COVID-19 severity in patients with spondyloarthritis: Results of the French RMD COVID-19 cohort

  2023

  ArticleJoint Bone Spine

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

Lieu de consultation

• APHM HOPITAUX SUD SAINTE MARGUERITE

  249 ET 270 — 270 Boulevard DE SAINTE MARGUERITE, 13274 Marseille 9e Arrondissement

  ☎ 0491380000Hospitalier🏥 Voir cet établissement

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

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

  Small-molecule factor B inhibitor for the treatment of complement-mediated diseases

  Proceedings of the National Academy of Sciences of the United States of America · 2019

  📚 179 citations🎯 RCR 8.50Top 3% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  Dysregulation of the alternative complement pathway (AP) predisposes individuals to a number of diseases including paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and C3 glomerulopathy. Moreover, glomerular Ig deposits can lead to complement-driven nephropathies. Here we describe the discovery of a highly potent, reversible, and selective small-molecule inhibitor of factor B, a serine protease that drives the central amplification loop of the AP. Oral administration of the inhibitor prevents KRN-induced arthritis in mice and is effective upon prophylactic and therapeutic dosing in an experimental model of membranous nephropathy in rats. In addition, inhibition of factor B prevents complement activation in sera from C3 glomerulopathy patients and the hemolysis of human PNH erythrocytes. These data demonstrate the potential therapeutic value of using a factor B inhibitor for systemic treatment of complement-mediated diseases and provide a basis for its clinical development.

• 2

  First flare of ACPA-positive rheumatoid arthritis after SARS-CoV-2 infection

  The Lancet. Rheumatology · 2021

  📚 60 citations🎯 RCR 3.96Top 11% NIH🔓 Open Access📄 PDF gratuit ↗
• 3

  Increased production of soluble CTLA-4 in patients with spondylarthropathies correlates with disease activity

  Arthritis research & therapy · 2009

  📚 43 citations🎯 RCR 1.11🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  Abstract Introduction Spondylarthropathies (SpA) are characterized by abnormal immune responses including T cell activation. Cytotoxic T lymphocyte associated molecule-4 (CTLA-4) is involved in down-regulating immune responses. A soluble form of CTLA-4 (sCTLA-4), resulting from an alternative splicing, has been identified and was found increased in several autoimmune diseases. Here, we evaluated circulating levels of sCTLA-4 as a marker of immune dysregulation in SpA. Intracellular CTLA-4 and levels of CTLA-4 transcript expression in peripheral blood lymphocytes (PBL) were also studied. Methods Sera from 165 patients with SpA were evaluated for sCTLA-4 measurements. Results were compared with those from 71 patients with rheumatoid arthritis (RA) and 88 healthy subjects. In 32 patients with SpA, 22 patients with RA and 15 healthy controls, we analyzed the intracellular CTLA-4 expression in CD4+ T cells, CD8+ T cells, activated (HLA-DR+Foxp3-) CD4+ T cells, CD4+ regulatory (CD25+Foxp3+) T cells and in CD3 negative cells by flow cytometry. Expression of the full length (coding for membrane CTLA-4) and spliced form (coding for sCTLA-4) of CTLA-4 transcripts in PBL were analyzed by quantitative real-time polymerase chain reaction (QRT-PCR). Results High levels of sCTLA-4 were found in the SpA group compared to the RA group and healthy controls (P < 0.0001). Soluble CTLA-4 serum levels strongly correlated with clinical index of disease activity BASDAI (r = 0.42, P < 0.0001) and C-reactive protein (CRP) levels (r = 0.17, P = 0.037). In contrast to RA patients, SpA patients did not exhibit changes in intracellular CTLA-4 expression in the different PBL subsets tested. Finally, the SpA group showed a preferential expression of the spliced CTLA-4 mRNA (P = 0.0014) in PBL. Conclusions SpA patients exhibit high levels of circulating sCTLA-4 that may result from an alternative splicing of CTLA-4 transcripts. This may influence immune activation and regulation in SpA.

Publications scientifiques (8) — classées par pathologie

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

Partager cette fiche