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A Role for STAT5 in the Pathogenesis of IL-2-Induced Glucocorticoid Resistance
Open accessAbstract
Glucocorticoids (GC) are highly effective in the control of diseases associated with T cell activation. However, a subset of individuals is GC insensitive. Previous studies have demonstrated that IL-2 can induce steroid resistance in mouse T cells. However, the mechanism for this phenomenon is unknown. In the current study we found that the murine cell line (HT-2) is steroid resistant when incubated with IL-2, but steroid sensitive when grown in IL-4. Furthermore, when HT-2 cells are treated with IL-2, the glucocorticoid receptor (GCR) does not translocate to the cell nucleus after dexamethasone treatment. In contrast, the GCR in IL-4-stimulated HT-2 cells does translocate into the cell nucleus after dexamethasone treatment. IL-2-induced steroid insensitivity in HT-2 cells appears to be a signaling event as the effects of IL-2 on nuclear translocation of the GCR occurred within 30 min even in the presence of cycloheximide. Indeed, preincubation of HT-2 cells with a Janus-associated kinase 3 inhibitor restored nuclear translocation of the GCR even in the presence of IL-2. Immunoprecipitation experiments revealed that phosphorylated STAT5 and GCR formed immune complexes. This association may lead to retardation of GCR nuclear translocation because IL-2 was not able to induce steroid insensitivity in splenocytes from STAT5 knockout mice. This study demonstrates a novel role for STAT5 in IL-2-induced steroid insensitivity.
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“inhibition of prednisolone-induced GR translocation, as well as GR-mediated gene transcription in human epidermal cells by TNF-α, is dependent on ERK activation.46”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [46]
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Metadata
- Authors
- Goleva, E., Kisich, K. O., & Leung, D. Y. M.
- Affiliations
- National Jewish Health (US)
- Corresponding author
- Goleva, Elena
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-11
- Volume
- 169
- Issue
- 10
- Pages
- 5934-5940
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2171016604
- Cited by
- 113
- References
- 37
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 1 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 8 · 2014: 3 · 2013: 7 · 2012: 5
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (HL37260, RR00051)
- National Heart, Lung, and Blood Institute (HL 36577, P01HL036577, HL 37260)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR 41256, R01AR041256)
- National Center for Research Resources (RR-00051)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- STAT5, glucocorticoid resistance, interleukin-2, glucocorticoid receptor, nuclear translocation, dexamethasone, IL-4, T cell activation, immune complex formation
- MeSH terms
- Animals, Cell Division, Cell Line, Cell Nucleus, Cells, Cultured, Dexamethasone, DNA-Binding Proteins, Drug Resistance, Enzyme Inhibitors, Interleukin-2, Mice, Inbred C57BL, Milk Proteins, Protein-Tyrosine Kinases, Receptors, Glucocorticoid, Spleen, T-Lymphocytes, Signal Transduction, Trans-Activators, Mice, Knockout, Dimerization, Active Transport, Cell Nucleus, STAT5 Transcription Factor, Mice, Janus Kinase 3
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