📇 Rhumatologue · NARBONNE · (11) · Libéral
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2 raisons identifiées
Praticien-chercheur
6 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
105.7 rhumatos / 100 000 hab. — département bien doté
✨ Génération du profil synthétique IA en cours…
CABINET DU DR Teodor BAN
12 RUE DU 1ER MAI, 11100 NARBONNE
Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
The Journal of clinical investigation · 1998
Nature communications · 2021
AbstractThe transcription factor IRF5 has been implicated as a therapeutic target for the autoimmune disease systemic lupus erythematosus (SLE). However, IRF5 activation status during the disease course and the effects of IRF5 inhibition after disease onset are unclear. Here, we show that SLE patients in both the active and remission phase have aberrant activation of IRF5 and interferon-stimulated genes. Partial inhibition of IRF5 is superior to full inhibition of type I interferon signaling in suppressing disease in a mouse model of SLE, possibly due to the function of IRF5 in oxidative phosphorylation. We further demonstrate that inhibition of IRF5 via conditional Irf5 deletion and a newly developed small-molecule inhibitor of IRF5 after disease onset suppresses disease progression and is effective for maintenance of remission in mice. These results suggest that IRF5 inhibition might overcome the limitations of current SLE therapies, thus promoting drug discovery research on IRF5 inhibitors.
International immunology · 2018
Abstract The transcription factor interferon regulatory factor-5 (IRF5) plays an important role in innate immune responses via the TLR-MyD88 (Toll-like receptor - myeloid differentiation primary response 88) pathway. IRF5 is also involved in the pathogenesis of the autoimmune disease systemic lupus erythematosus (SLE). Recent studies have identified new regulators, both positive and negative, which act on IRF5 activation events in the TLR-MyD88 pathway such as post-translational modifications, dimerization and nuclear translocation. A model of the causal relationship between IRF5 activation and SLE pathogenesis proposes that a loss of the negative regulation of IRF5 causes its hyperactivation, resulting in hyperproduction of type I interferons and other cytokines, and ultimately in the development of SLE. Importantly, to our knowledge, all murine models of SLE studied thus far have shown that IRF5 is required for the pathogenesis of SLE-like diseases. During the development of SLE-like diseases, IRF5 plays key roles in various cell types, including dendritic cells and B cells. It is noteworthy that the onset of SLE-like diseases can be inhibited by reducing the activity or amount of IRF5 by half. Therefore, IRF5 is an important therapeutic target of SLE, and selective suppression of its activity and expression may potentially lead to the development of new therapies.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Kidney & blood pressure research · 2024 · Journal Article
Ahn SY, Ko GJ, Hwang HS, Jeong KH, et al.
PloS one · 2023 · Journal Article
Ban TH, Choi BS, Yoon SA, Kim Y, et al.
The Journal of clinical investigation · 1998 · Journal Article
Nakamura N, Ban T, Yamaji K, Yoneda Y, et al.
Modern rheumatology · 2026 · Journal Article
Kanayama Y, Ban T, Sato GR, Arinuma Y, et al.
International immunology · 2018 · Journal Article
Ban T, Sato GR, Tamura T
Nature communications · 2021 · Journal Article
Ban T, Kikuchi M, Sato GR, Manabe A, et al.