The influence of glatiramer acetate on Th17-immune response in multiple sclerosis
Rattachement africain : ru. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Glatiramer acetate (GA) is approved for the treatment of multiple sclerosis (MS). However, the mechanism of action of GA in MS is still unclear. In particular, it is not known whether GA can modulate the pro-inflammatory Th17-type immune response in MS. We investigated the effects of original GA (Copaxone®, Teva, Israel) and generic GA (Timexone®, Biocad, Russia) on Th17- and Th1-type cytokine production in vitro in 25 patients with relapsing-remitting MS and 25 healthy subjects. Both original and generic GA at concentrations 50-200 μg/ml dose-dependently inhibited interleukin-17 and interferon-γ production by anti-CD3/anti-CD28-activated peripheral blood mononuclear cells from MS patients and healthy subjects. This effect of GA was reproduced using purified CD4+ T cells, suggesting that GA can directly modulate the functions of Th17 and Th1 cells. At high concentrations (100-200 μg/ml), GA also suppressed the production of Th17-differentiation cytokines (interleukin-1β and interleukin-6) by lipopolysaccharide (LPS)-activated dendritic cells (DCs). These GA/LPS-treated DCs induced lower interleukin-17 and interferon-γ production by autologous CD4+ T cells compared to LPS-treated DCs. These data suggest that GA can inhibit Th17-immune response and that this inhibitory effect is preferentially exercised by direct influence of GA on T cells. We also demonstrate a comparable ability of original and generic GA to modulate pro-inflammatory cytokine production.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- The influence of glatiramer acetate on Th17-immune response in multiple sclerosis
- Date Crossref
- 30/10/2020
- Éditeur
- Public Library of Science (PLoS)
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Pirogov Russian National Research Medical University Department of Neurology pays non établi dans la noticeUniversité ou école supérieure
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Federal Medical-Biological Agency Department of Neuroimmunology pays non établi dans la noticeOrganisme public
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Research Institute of Vaccines and Sera. Mechnikov of the Russian Academy of Medical Sciences pays non établi dans la noticeStructure de recherche
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Laboratory of Clinical Immunology pays non établi dans la noticeStructure de recherche
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Laboratory of Interferons pays non établi dans la noticeStructure de recherche
Department of Neurology — Pirogov Russian National Research Medical University, Department of Neuroimmunology — Federal Medical-Biological Agency et Research Institute of Vaccines and Sera. Mechnikov of the Russian Academy of Medical Sciences, avec 2 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.