📇 Rhumatologue · LES ABYMES · (971) · Salarié

M Jean-Pierre KARAM

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7 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
104 rhumatos / 100 000 hab. — département bien doté

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📍 LES ABYMES (971)SalariéRPPS 10101478385

14ans d'exercice (thèse 2012)·3 publications sur 5 ans↗

📊 Reconnaissance scientifique : 7/100📝 17 articles publiés🇫🇷 Publications académiques françaises (8)

✨ Génération du profil synthétique IA en cours…

Thèses universitaires

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

Jejunoileal bypass as a treatment of morbid obesity

Archives of internal medicine · 1977

📚 78 citations🎯 RCR 2.86

Immune checkpoint inhibitors-associated vasculitis: a heterogeneous condition with possible severe disease course

Rheumatology (Oxford, England) · 2025

📚 8 citations🎯 RCR 3.31🔓 Open Access

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Abstract Objective To describe presentation, treatment and outcome of immune checkpoint inhibitor (ICI) associated-vasculitis in cancer patients in a multicentre study. Methods Thanks to the ImmunoCancer International Registry (ICIR), a multidisciplinary network focused on the research of the immune related adverse events related to cancer immunotherapies, patients presenting with a clinical and/or radiological suspicion of vasculitis and histological evidence of vasculitis after being exposed to ICIs were retrospectively identified. Results Twenty-eight cases were identified in the ICIR registry. The median interval between starting ICI treatment and vasculitis diagnosis was 4 months. Small vessel vasculitis was predominant (n = 21), followed by large vessel (n = 4) and medium vessel (n = 3). The small vessel vasculitis included 10 unclassified vasculitis either with limited cutaneous involvement (n = 6) or systemic involvement (n = 4), five IgA vasculitis, three cryoglobulinemic vasculitis, and three ANCA+ vasculitis. At presentation or during the evolution, renal and neurologic manifestations were evidenced in seven cases each (25%). Renal biopsies documented immune glomerulopathies in six cases. Only seven patients (25%) fulfilled the 2022 ACR/EULAR classification criteria (four giant cell arteritis, two EGPA and one GPA). Most patients (90%) required systemic corticosteroid and an additional drug was given in 10 patients (36%). Vasculitis outcome was good: 22 patients had vasculitis complete response, no patient died due to vasculitis. Nine patients (32%) were rechallenged with immunotherapy with only one relapse. Conclusion ICI-associated vasculitis are rare, heterogeneous, but can be severe requiring urgent multidisciplinary management with aggressive treatment.

Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages

Cellular & molecular immunology · 2026

📚 1 citations🔓 Open Access📄 PDF gratuit ↗

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Abstract Rheumatoid arthritis (RA) exhibits heterogeneous endotypes, complicating treatment strategies. GM-CSF and GM-CSFRα are enriched in RA synovial CD68⁺macrophages (MΦs), and are implicated in acute and chronic disease stages. Since anti-TNFi and anti-IL6R therapies did not effectively suppress GM-CSF/GM-CSFRα expression or the GM-CSF-associated landscape, we explored alternative therapeutic strategies to target GM-CSF function using RA blood, synovial tissues, and preclinical models. We demonstrate that GM-CSF-MΦs reprogrammed in RA blood and synovial tissue share a distinct IL1β⁺S100A⁺HIF1⁺IL10ˡᵒNFIL3/6ˡᵒ expression profile, manifested by mitochondrial oxidative stress and fragmentation. To correct the metabolic imbalance of GM-CSF-MΦs, cells were treated with a complex I inhibitor (i) or a glucose uptake blocker. Complex Ii did not broadly alter the inflammatory or metabolic networks or affect the mitochondrial dynamics remodeled by GM-CSF-MΦs. While the glucose uptake inhibitor (HK2i) reduced glycolysis-derived ATP, it had limited efficacy in restricting the inflammatory signature or restoring TCA enzymes in GM-CSF-MΦs. In contrast, tofacitinib achieved broad-spectrum effects by downregulating GM-CSFRα expression and inhibiting STAT5 signaling. Moreover, tofacitinib redirected RA blood and synovial IL1β⁺S100A⁺HIF1⁺IL10ˡᵒNFIL3/6ˡᵒMΦs into a regulatory phenotype, reversing oxidative stress and mitochondrial fragmentation. In preclinical models, local GM-CSF overexpression induced MΦ-directed joint inflammation and metabolic dysregulation. Consistently, Tofacitinib reversed GM-CSF-differentiated murine IL1β⁺HBEGF⁺HIF1⁺MΦs by impeding STAT5 signaling, correcting metabolic dysregulation, and repairing mitochondrial fragmentation. In conclusion, anti-TNFi, anti-IL6R, and metabolic-targeted therapies were largely ineffective in modifying GM-CSF-MΦ pathology. Conversely, tofacitinib deactivation of STAT5 attenuates GM-CSF-MΦ-triggered inflammation and mitochondrial malfunction by restoring regulatory markers and rebalancing oxidative phosphorylation in RA specimens and/or preclinical models.

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M Jean-Pierre KARAM

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Thèses universitaires

Activité de recherche & publications

Publications académiques en France

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Top publications · les plus citées

Publications scientifiques (7) — classées par pathologie

Transversal5

Économie santé1

JAK inhibiteurs1

Qualité de vie / PROMs1

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