Methylprednisolone inhibits IFN-γ and IL-17 expression and production by cells infiltrating central nervous system in experimental autoimmune encephalomyelitis
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Background: Glucocorticoids have been shown to be effective in the treatment of autoimmune diseases of the CNS such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the mechanisms and the site of glucocorticoids' actions are still not completely defined. The aim of this study was to investigate the in vivo effect of the synthetic glucocorticoid methylprednisolone (MP) on the expression and production of proinflammatory cytokines interferon (IFN)-γ and interleukin (IL)-17 by cells infiltrating CNS tissue. Methods: Experimental autoimmune encephalomyelitis was induced in Dark Agouti (DA) rats by immunization with rat spinal cord homogenate mixed with adjuvants. Commencing on the day when the first EAE signs appeared, DA rats were injected daily for 3 days with MP and/or RU486, an antagonist of glucocorticoid receptor. Cytokine production and gene expression in CNS-infiltrating cells and lymph node cells were measured using ELISA and real time PCR, respectively. Results: Treatment of rats with MP ameliorated EAE, and the animals recovered without relapses. Further, MP inhibited IFN-γ and IL-17 expression and production in cells isolated from the CNS of DA rats with EAE after the last injection of MP. The observed effect of MP in vivo treatment was not mediated through depletion of CD4+ T cells among CNS infiltrating cells, or through induction of their apoptosis within the CNS. Finally, the glucocorticoid receptor-antagonist RU486 prevented the inhibitory effect of MP on IFN-γ and IL-17 production both in vitro and in vivo, thus indicating that the observed effects of MP were mediated through glucocorticoid receptor-dependent mechanisms. Conclusion: Taken together, these results demonstrate that amelioration of EAE by exogenous glucocorticoids might be, at least partly, ascribed to the limitation of effector cell functions in the target tissue.
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Methylprednisolone inhibits IL-17 production by lymphocytes.
“Methylprednisolone inhibits production of IL-17 by lymphocytes [179].”
From Steroidogenesis in the skin: Implications for local immune functions (2013) · cites this paper as [179]
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- Authors
- Miljković, Ž., Momčilović, M., Miljković, D., & Mostarica-Stojković, M.
- Affiliations
- University of Belgrade (RS)
- Corresponding author
- Momčilović, Miljana
- Venue
- Journal of Neuroinflammation
- Published
- 2009-12
- Volume
- 6
- Issue
- 1
- Pages
- 37-37
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC2797773
- OpenAlex
- W2035550266
- Cited by
- 35
- References
- 29
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 2 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2016: 1 · 2015: 4 · 2014: 3 · 2013: 8 · 2012: 5
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Digital Repository of Archived Publications (University of Belgrade, Institute for Biological Research Sinisa Stankovic) (submittedVersion)
- Funders
- Alexander von Humboldt-Stiftung
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- methylprednisolone, experimental autoimmune encephalomyelitis, glucocorticoids, interferon-gamma, IL-17, inflammatory cytokines, glucocorticoid receptor, RU486, multiple sclerosis, Dark Agouti rats, CD4+ T cells
- MeSH terms
- Animals, Central Nervous System, Encephalomyelitis, Autoimmune, Experimental, Glucocorticoids, Hormone Antagonists, Interferon-gamma, Methylprednisolone, Rats, Inbred Strains, Receptors, Glucocorticoid, Antigens, CD, Mifepristone, Interleukin-17, Rats
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