Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells

doi:10.1186/1471-2172-9-47

BMC Immunology

Volume 9

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Momčilović M
Miljković Ž
Popadić D
Marković M
Savić E
Ramić Z
Miljković D
Mostarica-Stojković M

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Momčilović M
Miljković Ž
Popadić D
Marković M
Savić E
Ramić Z
Miljković D
Mostarica-Stojković M
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Research article

Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells

Miljana Momčilović¹^* , Željka Miljković²^* , Dušan Popadić² , Miloš Marković² , Emina Savić² , Zorica Ramić² , Djordje Miljković¹ and Marija Mostarica-Stojković²

¹Department of Immunology, Institute for Biological Research "Siniša Stanković", Belgrade, Serbia

²Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Belgrade, Serbia

author email corresponding author email* Contributed equally

BMC Immunology 2008, 9:47doi:10.1186/1471-2172-9-47


Published:	12 August 2008

Abstract

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)-γ.

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-γT transcription factor expression, as well as Jun phosphorylation, but not ERK or p38 activation in mitogen-stimulated LNC. Importantly, MP collaborated with IFN-γ in inhibiting IL-17 generation in LNC.

Conclusion

The observed difference in the effect of MP on IL-17 and IFN-γ could be important for the understanding of the variability in the efficiency of glucocorticoids in the treatment of autoimmune diseases.