The BAFF/APRIL system in SLE pathogenesis.

Détails

Ressource 1Télécharger: R028 Vincent et al.pdf (2023.49 [Ko])
Etat: Public
Version: Author's accepted manuscript
Licence: Non spécifiée
ID Serval
serval:BIB_AEF919CB0373
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
The BAFF/APRIL system in SLE pathogenesis.
Périodique
Nature Reviews. Rheumatology
Auteur⸱e⸱s
Vincent F.B., Morand E.F., Schneider P., Mackay F.
ISSN
1759-4804 (Electronic)
ISSN-L
1759-4790
Statut éditorial
Publié
Date de publication
2014
Volume
10
Numéro
6
Pages
365-373
Langue
anglais
Résumé
Systemic lupus erythematosus (SLE) is characterized by multisystem immune-mediated injury in the setting of autoimmunity to nuclear antigens. The clinical heterogeneity of SLE, the absence of universally agreed clinical trial end points, and the paucity of validated therapeutic targets have, historically, contributed to a lack of novel treatments for SLE. However, in 2011, a therapeutic monoclonal antibody that neutralizes the cytokine TNF ligand superfamily member 13B (also known as B-cell-activating factor of the TNF family [BAFF]), belimumab, became the first targeted therapy for SLE to have efficacy in a randomized clinical trial. Because of its specificity, the efficacy of belimumab provides an opportunity to increase understanding of SLE pathophysiology. Although belimumab depletes B cells, this effect is not as powerful as that of other B-cell-directed therapies that have not been proven efficacious in randomized clinical trials. In this article, therefore, we review results suggesting that neutralizing BAFF can have effects on the immune system other than depletion of B cells. We also identify aspects of the BAFF system for which data in relation to SLE are still missing, and we suggest studies to investigate the pathogenesis of SLE and ways to refine anti-BAFF therapies. The role of a related cytokine, TNF ligand superfamily member 13 (also known as a proliferation-inducing ligand [APRIL]) in SLE is much less well understood, and hence this review focuses on BAFF.
Pubmed
Web of science
Création de la notice
10/07/2014 10:33
Dernière modification de la notice
18/01/2020 8:09
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