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Updated: Jul 2, 2026

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells
Miljana Momcilović1, Zeljka Miljković, Dusan Popadić
1Department of Immunology, Institute for Biological Research Sinisa Stanković, Belgrade, Serbia. mommilja@eunet.yu
Background:
Interleukin-17 (IL-17)-producing cells are increasingly considered to be the major pathogenic population in various autoimmune disorders. The effects of glucocorticoids, widely used as therapeutics for inflammatory and autoimmune disorders, on IL-17 generation have not been thoroughly investigated so far. Therefore, we have explored the influence of methylprednisolone (MP) on IL-17 expression in rat lymphocytes, and compared it to the effect of the drug on interferon (IFN)-gamma.
Results:
Production of IL-17 in mitogen-stimulated lymph node cells (LNC) from non-treated rats, as well as in myelin basic protein (MBP)-stimulated draining LNC from rats immunized with spinal cord homogenate and complete Freund's adjuvant was significantly reduced by MP. The reduction was dose-dependent, sustained through the follow-up period of 48 hours, and was not achieved through anti-proliferative effect. Additionally, MP inhibited IL-17 production in purified T cells as well, but to less extent than in LNC. In its influence on IL-17 production MP inhibited Ror-gammaT transcription factor expression, as well as Jun phosphorylation, but not ERK or p38 activation in mitogen-stimulated LNC. Importantly, MP collaborated with IFN-gamma in inhibiting IL-17 generation in LNC.
Conclusion:
The observed difference in the effect of MP on IL-17 and IFN-gamma could be important for the understanding of the variability in the efficiency of glucocorticoids in the treatment of autoimmune diseases.
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