The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Macrophage migration inhibitory factor promotes innate immune responses by suppressing glucocorticoid-induced expression of mitogen-activated protein kinase phosphatase-1
Abstract
The pro-inflammatory cytokine macrophage migration inhibitory factor (MIF) acts as a physiological counter-regulator of the immuno-suppressive effects of glucocorticoids. However, the mechanisms whereby MIF exerts its counter-balancing effect remain largely unknown. Here we report that MAPK phosphatase 1 (MKP-1), an archetypal member of dual specificity phosphatase that inactivates MAPK activity in response to pro-inflammatory stimuli, is a critical target of MIF-glucocorticoid crosstalk. Recombinant MIF counter-regulated in a dose-dependent fashion dexamethasone inhibition of TNF and IL-8 production by RAW 264.7 macrophages and U-937 promonocytes stimulated with lipopolysaccharides (LPS) or with LPS plus phorbol 12-myristate 13-acetate. Stimulation of RAW 264.7 macrophages with dexamethasone or dexamethasone plus LPS led to a robust up-regulation of MKP-1 mRNA and protein expressions that were counter-regulated by addition of recombinant MIF. Antisense MIF macrophages expressing reduced levels of endogenous MIF produced higher amount of MKP-1 and lower amount of TNF after exposure to dexamethasone and dexamethasone plus LPS, indicating that endogenous MIF acts in an autocrine fashion to override glucocorticoid-induced MKP-1 expression and inhibition of cytokine production. Taken together, these data identify MKP-1 as a molecular target of MIF-glucocorticoid crosstalk and provide a molecular basis for the control of macrophage responses by a pair of physiological regulators of innate immunity.
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“Acute GC exposure induces sustained expression of MKP-1 in a variety of cells including macrophages (Roger et al., 2005).”
From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Roger et al., 2005
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Cites
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NF-κB regulation in the immune system
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Macrophage migration inhibitory factor: a regulator of innate immunity
Calandra, T., & Roger, T. (2003) · Nature reviews. Immunology · doi:10.1038/nri1200 · Cited by 1,782
Detection of circulating tumor necrosis factor after endotoxin administration
Michie, H. R., Manogue, K. R., Spriggs, D. R., Revhaug, A., O'Dwyer, S., Dinarello, C. A., Cerami, A., Wolff, S. M., & Wilmore, D. W. (1988) · New England Journal of Medicine · doi:10.1056/nejm198806093182301 · Cited by 1,677
Role of Transcriptional Activation of IκBα in Mediation of Immunosuppression by Glucocorticoids
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Cited by
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Glucocorticoid resistance in inflammatory diseases
Barnes, P. J., & Adcock, I. M. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60326-3 · Cited by 983
Cytokines in Sepsis: Potent Immunoregulators and Potential Therapeutic Targets—An Updated View
Schulte, W., Bernhagen, J., & Bucala, R. (2013) · Mediators of Inflammation · doi:10.1155/2013/165974 · Cited by 782
“MIF’s critical role within the immune system is further underscored by the finding that MIF is induced by low concentrations of glucocorticoids and has the unique ability to override the anti-inflammatory and immunosuppressive effects of glucocorticoids [77, 81, 84].”
BackgroundCorticosteroid resistance in patients with asthma and chronic obstructive pulmonary disease
Barnes, P. J. (2013) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2012.12.1564 · Cited by 708
“It is induced by corticosteroids and appears to inhibit their anti-inflammatory effects, mainly through inhibiting the induction ofMKP-1.(81)Macrophage migration inhibitory factor has also been implicated in the pathogenesis of allergic inflammation inmousemodels of asthma(82) and in the steroid resistance of asthmati…”
BackgroundMAPK phosphatases — regulating the immune response
Liu, Y., Shepherd, E. G., & Nelin, L. D. (2007) · Nature reviews. Immunology · doi:10.1038/nri2035 · Cited by 679
“found that MIF alleviated the inhibitory effect of dexamethasone on TNF and CXC-chemokine ligand 8 (CXCL8; also known as IL-8) production in a dose-dependent manne”
BackgroundGlucocorticosteroids: current and future directions
Barnes, P. J. (2010) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2010.01199.x · Cited by 550
Metadata
- Authors
- Roger, T., Chanson, A., Knaup‐Reymond, M., & Calandra, T.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- Corresponding author
- Calandra, Thierry
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2005-12
- Volume
- 35
- Issue
- 12
- Pages
- 3405-3413
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- OpenAlex
- W2046525356
- Cited by
- 184
- References
- 48
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 6 · 2022: 6 · 2021: 7 · 2020: 4 · 2019: 13 · 2018: 8 · 2017: 7 · 2016: 8 · 2015: 4 · 2014: 9 · 2013: 10 · 2012: 16
- FWCI
- 4.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Macrophage Migration Inhibitory Factor
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- macrophage migration inhibitory factor, MAPK phosphatase-1, glucocorticoids, dexamethasone, innate immunity, macrophages, lipopolysaccharide, TNF-α, interleukin-8, autocrine regulation, dual-specificity phosphatase, MAPK signaling, immunosuppression
- MeSH terms
- Animals, Cell Line, Glucocorticoids, Humans, Immunity, Innate, Macrophage Migration-Inhibitory Factors, Phosphoprotein Phosphatases, Cytokines, Protein Tyrosine Phosphatases, Immediate-Early Proteins, Cell Cycle Proteins, U937 Cells, Mice, Dual Specificity Phosphatase 1, Protein Phosphatase 1
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