MME ANNIE PELLERIN

Rhumatologue

RPPS 10001791077

📊 Reconnaissance scientifique : 7/100📝 19 articles publiés

✨ Génération du profil synthétique IA en cours…

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Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.

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7 articles ont été cités au moins 7fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.

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Top publications · les plus citées

Monoclonal antibody targeting BDCA2 ameliorates skin lesions in systemic lupus erythematosus

The Journal of clinical investigation · 2019

📚 208 citations🎯 RCR 8.63Top 3% NIH🩺 Clinique🔓 Open Access📄 PDF gratuit ↗

Anti-BDCA2 monoclonal antibody inhibits plasmacytoid dendritic cell activation through Fc-dependent and Fc-independent mechanisms

EMBO molecular medicine · 2015

📚 96 citations🎯 RCR 2.97Top 16% NIH🔓 Open Access📄 PDF gratuit ↗

Lire l'abstract Crossref ↓

Abstract Type I interferons (IFN‐I) are implicated in the pathogenesis of systemic lupus erythematosus (SLE). In SLE, immune complexes bind to the CD32a (FcγRIIa) receptor on the surface of plasmacytoid dendritic cells (pDCs) and stimulate the secretion of IFN‐I from pDCs. BDCA2 is a pDC‐specific receptor that, when engaged, inhibits the production of IFN‐I in human pDCs. BDCA2 engagement, therefore, represents an attractive therapeutic target for inhibiting pDC‐derived IFN‐I and may be an effective therapy for the treatment of SLE. In this study, we show that 24F4A, a humanized monoclonal antibody (mAb) against BDCA2, engages BDCA2 and leads to its internalization and the consequent inhibition of TLR‐induced IFN‐I by pDCs in vitro using blood from both healthy and SLE donors. These effects were confirmed in vivo using a single injection of 24F4A in cynomolgus monkeys. 24F4A also inhibited pDC activation by SLE‐associated immune complexes (IC). In addition to the inhibitory effect of 24F4A through engagement of BDCA2, the Fc region of 24F4A was critical for potent inhibition of IC‐induced IFN‐I production through internalization of CD32a. This study highlights the novel therapeutic potential of an effector‐competent anti‐BDCA2 mAb that demonstrates a dual mechanism to dampen pDC responses for enhanced clinical efficacy in SLE.

Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNα Production From Patients Affected With Cutaneous Lupus Erythematosus

Frontiers in immunology · 2019

📚 30 citations🎯 RCR 1.30🔓 Open Access

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Publications scientifiques (9) — classées par pathologie

Transversal3

Lupus2

Pédiatrie2

AINS1

csDMARDs1

Génétique1

Pharmacovigilance1

Sjögren1

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