The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
IL-6 blockade inhibits the induction of myelin antigen-specific Th17 cells and Th1 cells in experimental autoimmune encephalomyelitis
Open accessAbstract
The development of Th17 cells is a key event in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), a murine model of human multiple sclerosis (MS). Previous studies have demonstrated that an IL-6-dependent pathway is involved in the differentiation of Th17 cells from naïve CD4-positive T cells in vitro. However, the role of IL-6 in vivo in the development of Th17 cells in EAE has remained unclear. In the present study, we found that IL-6 blockade by treatment with an anti-IL-6 receptor monoclonal antibody (anti-IL-6R mAb) inhibited the development of EAE and inhibited the induction of myelin oligodendrocyte glycoprotein (MOG) peptide-specific CD4-positive, CD8-positive, and Th17 T cells, in inguinal lymph nodes. Thus, the protective effect of IL-6 blockade in EAE is likely to be mediated via the inhibition of the development of MOG-peptide-specific Th17 cells and Th1 cells, which in turn leads to reduced infiltration of T cells into the CNS. These findings indicate that anti-IL-6R mAb treatment might represent a novel therapy for human MS.
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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Transforming growth factor-β induces development of the TH17 lineage
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
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IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis
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Cited by
IL‐6 in inflammation, immunity, and disease
Tanaka, T., Narazaki, M., & Kishimoto, T. (2014) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a016295 · Cited by 5,046
Self-citationInterleukin-17 and Type 17 Helper T Cells
Miossec, P., Korn, T., & Kuchroo, V. K. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0707449 · Cited by 1,409
Treg cell-based therapies: challenges and perspectives
Raffin, C., Vo, L. T., & Bluestone, J. A. (2020) · Nature Reviews Immunology · doi:10.1038/s41577-019-0232-6 · Cited by 720
The role of interleukin-6 signaling in nervous tissue
Rothaug, M., Becker-Pauly, C., & Rose-John, S. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.03.018 · Cited by 491
Trans-presentation of IL-6 by dendritic cells is required for the priming of pathogenic TH17 cells
Heink, S., Yogev, N., Garbers, C., Herwerth, M., Aly, L., Gasperi, C., Husterer, V., Croxford, A. L., Möller-Hackbarth, K., Bartsch, H. S., et al. (2017) · Nature Immunology · doi:10.1038/ni.3632 · Cited by 386
Metadata
- Authors
- Serada, S., Fujimoto, M., Mihara, M., Koike, N., Ohsugi, Y., Nomura, S., Yoshida, H., Nishikawa, T., Terabe, F., Ohkawara, T., Takahashi, T., Ripley, B., Kimura, A., Kishimoto, T., & Naka, T.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2008-07
- Volume
- 105
- Issue
- 26
- Pages
- 9041-9046
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2051474906
- Cited by
- 349
- References
- 12
- FWCI
- 19.17
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: IL-6 blockade inhibits the induction of myelin antigen-specific Th17 cells and Th1 cells in experimental autoimmune encephalomyelitis. https://app.cochat.ai/papers/10.1073/pnas.0802218105
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- Serada, S., Fujimoto, M., Mihara, M., Koike, N., Ohsugi, Y., Nomura, S., Yoshida, H., Nishikawa, T., Terabe, F., Ohkawara, T., Takahashi, T., Ripley, B., Kimura, A., Kishimoto, T., & Naka, T. (2008). IL-6 blockade inhibits the induction of myelin antigen-specific Th17 cells and Th1 cells in experimental autoimmune encephalomyelitis. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0802218105
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.