ArticleImmunology2014
Endogenous interleukin-6 amplifies interleukin-17 production and corticoid-resistance in peripheral T cells from patients with multiple sclerosis.
Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Challenges and advances in the management of inflammation in atherosclerosis.Journal of advanced research · 2025Review
- Corticosteroid-depending effects on peripheral immune cell subsets vary according to disease modifying strategies in multiple sclerosis.Frontiers in immunology · 2024Article
- Review
- Exploring the impact of ketogenic diet on multiple sclerosis: obesity, anxiety, depression, and the glutamate system.Frontiers in nutrition · 2023Review
- Steroid-Refractory Gut Graft-Versus-Host Disease: What We Have Learned From Basic Immunology and Experimental Mouse Model.Frontiers in immunology · 2022Review
- Body Mass Index, Interleukin-6 Signaling and Multiple Sclerosis: A Mendelian Randomization Study.Frontiers in immunology · 2022Article
- Article
- Cytokines and Transgenic Matrix in Autoimmune Diseases: Similarities and Differences.Biomedicines · 2020Review
- Anti-inflammatory effects of dietary vitamin DNeurology. Genetics · 2018Article
- Differential effects of diesel exhaust particles on T cell differentiation and autoimmune disease.Particle and fibre toxicology · 2018Article
- Different interleukin-17-secreting Toll-like receptorImmunology · 2018Article
- Review
- IL-34 Upregulated Th17 Production through Increased IL-6 Expression by Rheumatoid Fibroblast-Like Synoviocytes.Mediators of inflammation · 2017Article
- A gradient of glucocorticoid sensitivity among helper T cell cytokines.Cytokine & growth factor reviews · 2016Review
- GWAS analysis implicates NF-κB-mediated induction of inflammatory T cells in multiple sclerosis.Genes and immunity · 2016Article
- Article
- Intracranial delivery of interleukin-17A via adeno-associated virus fails to induce physical and learning disabilities and neuroinflammation in mice but improves glucose metabolism through AKT signaling pathway.Brain, behavior, and immunity · 2016Article
- Blockade of interleukin-6 receptor enhances the anti-arthritic effect of glucocorticoids without decreasing bone mineral density in mice with collagen-induced arthritis.Clinical and experimental immunology · 2015Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) has been implicated in the induction of pathogenic IL-17-producing T cells in autoimmune diseases, and studies evaluating the role of this cytokine in T-cell function in patients with multiple sclerosis (MS) are lacking. Our objective was to evaluate the role of IL-6 receptor (IL-6R) signalling on in vitro functional status of T cells from patients with relapsing-remitting MS during clinical remission. Our results demonstrated that, even during the remission phase, activated T cells from patients produce higher levels of IL-17, and this cytokine was positively correlated with disease severity, as determined by Expanded Disability Status Scale score. In the MS group, the blockade of IL-6R signalling by anti-IL-6R monoclonal antibody reduced IL-17 production and elevated IL-10 release by activated CD4(+) T cells, but it did not alter the production of these cytokines by activated CD8(+) T cells. Blockade of IL-6R signalling also reduced the ability of monocytes to up-regulate T helper type 17 phenotype in patients with MS. Finally, both cell proliferation and IL-17 release by CD4(+) and, mainly, CD8(+) T cells from patients with MS were less sensitive to hydrocortisone inhibition than control group. Interestingly, IL-6R signalling blockade restored the ability of hydrocortisone to inhibit both T-cell proliferation and IL-17 production. Collectively, these results suggest that IL-6 might be involved in MS pathogenesis by enhancing IL-17 production and reducing corticoid inhibitory effects on activated T cells.
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