Type 1 interferon suppresses expression and glucocorticoid induction of glucocorticoid-induced leucine zipper (GILZ)

SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer...

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Published inFrontiers in immunology Vol. 13; p. 1034880
Main Authors Dankers, Wendy, Northcott, Melissa, Bennett, Taylah, D'Cruz, Akshay, Sherlock, Rochelle, Gearing, Linden J, Hertzog, Paul, Russ, Brendan, Miceli, Iolanda, Scheer, Sebastian, Fujishiro, Maki, Hayakawa, Kunihiro, Ikeda, Keigo, Morand, Eric F, Jones, Sarah A
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LanguageEnglish
Published Switzerland Frontiers Media S.A 23.11.2022
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Abstract SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used and respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.
AbstractList SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed in vitro experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used in vivo and in vitro respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in vitro in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.
SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed in vitro experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used in vivo and in vitro respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in vitro in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed in vitro experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used in vivo and in vitro respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in vitro in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.
SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used and respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.
SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed in vitro experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used in vivo and in vitro respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in vitro in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.
Author D'Cruz, Akshay
Ikeda, Keigo
Jones, Sarah A
Hertzog, Paul
Hayakawa, Kunihiro
Bennett, Taylah
Morand, Eric F
Gearing, Linden J
Miceli, Iolanda
Dankers, Wendy
Russ, Brendan
Northcott, Melissa
Scheer, Sebastian
Sherlock, Rochelle
Fujishiro, Maki
AuthorAffiliation 1 Centre for Inflammatory Diseases, Monash University , Melbourne, VIC , Australia
3 Institutes for Environmental and Gender Specific Medicine, Juntendo University Graduate School of Medicine , Chiba , Japan
2 Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research , Melbourne, VIC , Australia
4 Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital , Chiba , Japan
AuthorAffiliation_xml – name: 1 Centre for Inflammatory Diseases, Monash University , Melbourne, VIC , Australia
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Cites_doi 10.4049/jimmunol.1202662
10.1096/fj.14-254755
10.1186/s12865-017-0225-9
10.1016/j.jaut.2015.05.010
10.1016/j.febslet.2011.07.043
10.1016/j.bbi.2009.01.001
10.1016/S2665-9913(19)30105-5
10.1084/jem.20021553
10.1074/jbc.M101522200
10.1128/MCB.22.22.7929-7941.2002
10.1172/JCI30724
10.1056/NEJMoa1912196
10.1038/nature11232
10.4238/2013.February.19.1
10.1111/j.1600-065X.2008.00630.x
10.1016/j.physbeh.2015.12.013
10.1038/383726a0
10.1136/lupus-2021-000625
10.1182/blood.V98.3.743
10.1002/art.37858
10.1016/S2665-9913(21)00006-0
10.1096/fj.15-273664
10.1021/acs.jmedchem.8b00917
10.1002/art.39950
10.4049/jimmunol.181.12.8761
10.1016/S1074-7613(00)80398-2
10.1002/art.39962
10.1006/meth.2001.1262
10.1136/lupus-2018-000270
10.1002/art.34473
10.1038/nature09102
10.1136/annrheumdis-2015-207744
10.3389/fimmu.2021.652800
10.1093/rheumatology/kew431
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Keywords GILZ
glucocorticoid
systemic lupus erythematosus (SLE)
autoimmunity
STAT1
inflammation
interferon
Language English
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content type line 23
These authors share senior authorship
Edited by: Trine N. Jorgensen, Case Western Reserve University, United States
This article was submitted to Autoimmune and Autoinflammatory Disorders: Autoimmune Disorders, a section of the journal Frontiers in Immunology
These authors share first authorship
Reviewed by: Simona Ronchetti, University of Perugia, Italy; Andreia C. Lino, German Rheumatism Research Center (DRFZ), Germany
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References Psarras (B4) 2017; 56
Mittelstadt (B24) 2001; 276
Chavele (B30) 2011; 585
Livak (B14) 2001; 25
Petri (B1) 2012; 64
Felger (B22) 2016; 166
Crispín (B29) 2008; 181
Ayroldi E (B23) 2001; 98
Thurman (B19) 2012; 489
Bennett (B3) 2003; 197
Hoffman (B15) 2017; 69
Ayroldi (B26) 2007; 117
Jones (B12) 2016; 75
Fensome (B18) 2018; 61
Ayroldi (B25) 2002; 22
Barrat (B6) 2008; 223
Northcott (B9) 2021; 3
Guiducci (B8) 2010; 465
Ayroldi (B10) 2014; 28
Jones (B31) 2015; 61
Nataraja (B13) 2021; 12
Apostolopoulos (B2) 2020; 2
Furie (B16) 2017; 69
Northcott (B20) 2022; 9
Cheng (B28) 2013; 31
Ikeda (B17) 2017; 18
Stöcklin (B33) 1996; 383
Ronnblom (B7) 2019; 6
Yang (B32) 2015; 29
Morand (B5) 2020; 382
Hu (B34) 2009; 23
Melo (B21) 2013; 12
D’Adamio (B11) 1997; 7
Ngo (B27) 2013; 65
References_xml – volume: 31
  year: 2013
  ident: B28
  article-title: GILZ overexpression inhibits endothelial cell adhesive function through regulation ofNF-κB and MAPK activity
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1202662
  contributor:
    fullname: Cheng
– volume: 28
  year: 2014
  ident: B10
  article-title: Targeting glucocorticoid side effects: selective glucocorticoid receptor modulator or glucocorticoid-induced leucine zipper? a perspective
  publication-title: FASEB journal: Off Publ Fed Am Societies Exp Biol
  doi: 10.1096/fj.14-254755
  contributor:
    fullname: Ayroldi
– volume: 18
  start-page: 41
  year: 2017
  ident: B17
  article-title: JAK inhibitor has the amelioration effect in lupus-prone mice: The involvement of IFN signature gene downregulation
  publication-title: BMC Immunol
  doi: 10.1186/s12865-017-0225-9
  contributor:
    fullname: Ikeda
– volume: 61
  start-page: 73
  year: 2015
  ident: B31
  article-title: GILZ regulates Th17 responses and restrains IL-17-mediated skin inflammation
  publication-title: J Autoimmun
  doi: 10.1016/j.jaut.2015.05.010
  contributor:
    fullname: Jones
– volume: 585
  year: 2011
  ident: B30
  article-title: Regulatory T-cells in systemic lupus erythematosus and rheumatoid arthritis
  publication-title: FEBS letters.
  doi: 10.1016/j.febslet.2011.07.043
  contributor:
    fullname: Chavele
– volume: 23
  year: 2009
  ident: B34
  article-title: Interferon-alpha inhibits glucocorticoid receptor-mediated gene transcription via STAT5 activation in mouse HT22 cells
  publication-title: Brain behavior Immun
  doi: 10.1016/j.bbi.2009.01.001
  contributor:
    fullname: Hu
– volume: 2
  year: 2020
  ident: B2
  article-title: Factors associated with damage accrual in patients with systemic lupus erythematosus with no clinical or serological disease activity: a multicentre cohort study
  publication-title: Lancet Rheumatol
  doi: 10.1016/S2665-9913(19)30105-5
  contributor:
    fullname: Apostolopoulos
– volume: 197
  year: 2003
  ident: B3
  article-title: Interferon and granulopoiesis signatures in systemic lupus erythematosus blood
  publication-title: J Exp Med
  doi: 10.1084/jem.20021553
  contributor:
    fullname: Bennett
– volume: 276
  year: 2001
  ident: B24
  article-title: Inhibition of AP-1 by the glucocorticoid-inducible protein GILZ
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M101522200
  contributor:
    fullname: Mittelstadt
– volume: 22
  year: 2002
  ident: B25
  article-title: Glucocorticoid-induced leucine zipper inhibits the raf-extracellular signal-regulated kinase pathway by binding to raf-1
  publication-title: Mol Cell Biol
  doi: 10.1128/MCB.22.22.7929-7941.2002
  contributor:
    fullname: Ayroldi
– volume: 117
  year: 2007
  ident: B26
  article-title: GILZ mediates the antiproliferative activity of glucocorticoids by negative regulation of ras signaling
  publication-title: J Clin Invest.
  doi: 10.1172/JCI30724
  contributor:
    fullname: Ayroldi
– volume: 382
  year: 2020
  ident: B5
  article-title: Trial of anifrolumab in active systemic lupus erythematosus
  publication-title: New Engl J Med
  doi: 10.1056/NEJMoa1912196
  contributor:
    fullname: Morand
– volume: 489
  start-page: 75
  year: 2012
  ident: B19
  article-title: The accessible chromatin landscape of the human genome
  publication-title: Nature
  doi: 10.1038/nature11232
  contributor:
    fullname: Thurman
– volume: 12
  year: 2013
  ident: B21
  article-title: Persistent glucocorticoid resistance in systemic lupus erythematosus patients during clinical remission
  publication-title: Genet Mol research: GMR.
  doi: 10.4238/2013.February.19.1
  contributor:
    fullname: Melo
– volume: 223
  year: 2008
  ident: B6
  article-title: Development of TLR inhibitors for the treatment of autoimmune diseases
  publication-title: Immunol Rev
  doi: 10.1111/j.1600-065X.2008.00630.x
  contributor:
    fullname: Barrat
– volume: 166
  start-page: 14
  year: 2016
  ident: B22
  article-title: Interferon-alpha-induced inflammation is associated with reduced glucocorticoid negative feedback sensitivity and depression in patients with hepatitis c virus
  publication-title: Physiol behavior.
  doi: 10.1016/j.physbeh.2015.12.013
  contributor:
    fullname: Felger
– volume: 383
  year: 1996
  ident: B33
  article-title: Functional interactions between Stat5 and the glucocorticoid receptor
  publication-title: Nature
  doi: 10.1038/383726a0
  contributor:
    fullname: Stöcklin
– volume: 9
  start-page: e000625
  year: 2022
  ident: B20
  article-title: Type 1 interferon status in systemic lupus erythematosus: a longitudinal analysis
  publication-title: Lupus Sci Med
  doi: 10.1136/lupus-2021-000625
  contributor:
    fullname: Northcott
– volume: 98
  year: 2001
  ident: B23
  article-title: Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor kappaB
  publication-title: Blood.
  doi: 10.1182/blood.V98.3.743
  contributor:
    fullname: Ayroldi E
– volume: 65
  year: 2013
  ident: B27
  article-title: Divergent effects of endogenous and exogenous GILZ in models of inflammation and arthritis
  publication-title: Arthritis Rheumatism.
  doi: 10.1002/art.37858
  contributor:
    fullname: Ngo
– volume: 3
  year: 2021
  ident: B9
  article-title: Glucocorticoid gene signatures in systemic lupus erythematosus and the effects of type I interferon: a cross-sectional and in-vitro study
  publication-title: Lancet Rheumatol
  doi: 10.1016/S2665-9913(21)00006-0
  contributor:
    fullname: Northcott
– volume: 29
  year: 2015
  ident: B32
  article-title: Crosstalk between bone marrow-derived mesenchymal stem cells and regulatory T cells through a glucocorticoid-induced leucine zipper/developmental endothelial locus-1-dependent mechanism
  publication-title: FASEB journal: Off Publ Fed Am Societies Exp Biol
  doi: 10.1096/fj.15-273664
  contributor:
    fullname: Yang
– volume: 61
  year: 2018
  ident: B18
  article-title: Dual inhibition of TYK2 and JAK1 for the treatment of autoimmune diseases: Discovery of ((S)-2,2-Difluorocyclopropyl)((1 R,5 s)-3-(2-((1-methyl-1 h-pyrazol-4-yl)amino)pyrimidin-4-yl)-3,8-diazabicyclo[3.2.1]octan-8-yl)methanone (PF-06700841)
  publication-title: J Med Chem
  doi: 10.1021/acs.jmedchem.8b00917
  contributor:
    fullname: Fensome
– volume: 69
  year: 2017
  ident: B15
  article-title: Gene expression and pharmacodynamic changes in 1,760 systemic lupus erythematosus patients from two phase III trials of BAFF blockade with tabalumab
  publication-title: Arthritis Rheumatol
  doi: 10.1002/art.39950
  contributor:
    fullname: Hoffman
– volume: 181
  year: 2008
  ident: B29
  article-title: Expanded double negative T cells in patients with systemic lupus erythematosus produce IL-17 and infiltrate the kidneys
  publication-title: J Immunol (Baltimore Md: 1950).
  doi: 10.4049/jimmunol.181.12.8761
  contributor:
    fullname: Crispín
– volume: 7
  year: 1997
  ident: B11
  article-title: A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death
  publication-title: Immunity.
  doi: 10.1016/S1074-7613(00)80398-2
  contributor:
    fullname: D’Adamio
– volume: 69
  year: 2017
  ident: B16
  article-title: Anifrolumab, an anti-interferon-alpha receptor monoclonal antibody, in moderate-to-Severe systemic lupus erythematosus
  publication-title: Arthritis Rheumatol (Hoboken NJ)
  doi: 10.1002/art.39962
  contributor:
    fullname: Furie
– volume: 25
  year: 2001
  ident: B14
  article-title: Analysis of relative gene expression data using real-time quantitative PCR and the 2[-delta delta C(T)] method
  publication-title: Methods.
  doi: 10.1006/meth.2001.1262
  contributor:
    fullname: Livak
– volume: 6
  year: 2019
  ident: B7
  article-title: Interferon pathway in SLE: one key to unlocking the mystery of the disease
  publication-title: Lupus Sci Med
  doi: 10.1136/lupus-2018-000270
  contributor:
    fullname: Ronnblom
– volume: 64
  year: 2012
  ident: B1
  article-title: Derivation and validation of systemic lupus international collaborating clinics classification criteria for systemic lupus erythematosus
  publication-title: Arthritis rheumatism.
  doi: 10.1002/art.34473
  contributor:
    fullname: Petri
– volume: 465
  year: 2010
  ident: B8
  article-title: TLR recognition of self nucleic acids hampers glucocorticoid activity in lupus
  publication-title: Nature
  doi: 10.1038/nature09102
  contributor:
    fullname: Guiducci
– volume: 75
  year: 2016
  ident: B12
  article-title: Glucocorticoid-induced leucine zipper (GILZ) inhibits b cell activation in systemic lupus erythematosus
  publication-title: Ann Rheum Dis
  doi: 10.1136/annrheumdis-2015-207744
  contributor:
    fullname: Jones
– volume: 12
  year: 2021
  ident: B13
  article-title: GILZ regulates the expression of pro-inflammatory cytokines and protects against end-organ damage in a model of lupus
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2021.652800
  contributor:
    fullname: Nataraja
– volume: 56
  year: 2017
  ident: B4
  article-title: Type I interferon-mediated autoimmune diseases: pathogenesis, diagnosis and targeted therapy
  publication-title: Rheumatol (Oxford England).
  doi: 10.1093/rheumatology/kew431
  contributor:
    fullname: Psarras
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Snippet SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for...
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SubjectTerms GILZ
glucocorticoid
Glucocorticoids - pharmacology
Humans
Immunology
inflammation
interferon
Interferon Type I
Janus Kinase Inhibitors
Janus Kinases
Leucine Zippers
Leukocytes, Mononuclear
Quality of Life
Signal Transduction
STAT Transcription Factors
STAT1
systemic lupus erythematosus (SLE)
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Title Type 1 interferon suppresses expression and glucocorticoid induction of glucocorticoid-induced leucine zipper (GILZ)
URI https://www.ncbi.nlm.nih.gov/pubmed/36505447
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https://doaj.org/article/3505bf1850804a299c6894502a57d398
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