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Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells
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 in...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2525626/ https://www.ncbi.nlm.nih.gov/pubmed/18700009 http://dx.doi.org/10.1186/1471-2172-9-47 |
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author | Momčilović, Miljana Miljković, Željka Popadić, Dušan Marković, Miloš Savić, Emina Ramić, Zorica Miljković, Djordje Mostarica-Stojković, Marija |
author_facet | Momčilović, Miljana Miljković, Željka Popadić, Dušan Marković, Miloš Savić, Emina Ramić, Zorica Miljković, Djordje Mostarica-Stojković, Marija |
author_sort | Momčilović, Miljana |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2525626 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-25256262008-08-27 Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells Momčilović, Miljana Miljković, Željka Popadić, Dušan Marković, Miloš Savić, Emina Ramić, Zorica Miljković, Djordje Mostarica-Stojković, Marija BMC Immunol Research Article 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. BioMed Central 2008-08-12 /pmc/articles/PMC2525626/ /pubmed/18700009 http://dx.doi.org/10.1186/1471-2172-9-47 Text en Copyright © 2008 Momčilović et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Momčilović, Miljana Miljković, Željka Popadić, Dušan Marković, Miloš Savić, Emina Ramić, Zorica Miljković, Djordje Mostarica-Stojković, Marija Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells |
title | Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells |
title_full | Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells |
title_fullStr | Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells |
title_full_unstemmed | Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells |
title_short | Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells |
title_sort | methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed t cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2525626/ https://www.ncbi.nlm.nih.gov/pubmed/18700009 http://dx.doi.org/10.1186/1471-2172-9-47 |
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