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Article ; Online: The key role of the lymph node niche in the development of rheumatoid arthritis.

Jiménez-Martínez, Marina / Dankers, Wendy / van Baarsen, Lisa G M

2023 Volume 91, Issue 2, Page(s) 105661

MeSH term(s)	Humans ; Arthritis, Rheumatoid/pathology ; Lymph Nodes/pathology
Language	English
Publishing date	2023-11-15
Publishing country	France
Document type	Editorial
ZDB-ID	2020487-5
ISSN	1778-7254 ; 1297-319X
ISSN (online)	1778-7254
ISSN	1297-319X
DOI	10.1016/j.jbspin.2023.105661
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Article ; Online: Could GILZ Be the Answer to Glucocorticoid Toxicity in Lupus?

Flynn, Jacqueline K / Dankers, Wendy / Morand, Eric F

Frontiers in immunology

2019 Volume 10, Page(s) 1684

Abstract: Glucocorticoids (GC) are used globally to treat autoimmune and inflammatory disorders. Their anti-inflammatory actions are mainly mediated via binding to the glucocorticoid receptor (GR), creating a GC/GR complex, which acts in both the cytoplasm and ... ...

Abstract	Glucocorticoids (GC) are used globally to treat autoimmune and inflammatory disorders. Their anti-inflammatory actions are mainly mediated via binding to the glucocorticoid receptor (GR), creating a GC/GR complex, which acts in both the cytoplasm and nucleus to regulate the transcription of a host of target genes. As a result, signaling pathways such as NF-κB and AP-1 are inhibited, and cell activation, differentiation and survival and cytokine and chemokine production are suppressed. However, the gene regulation by GC can also cause severe side effects in patients. Systemic lupus erythematosus (SLE or lupus) is a multisystem autoimmune disease, characterized by a poorly regulated immune response leading to chronic inflammation and dysfunction of multiple organs, for which GC is the major current therapy. Long-term GC use, however, can cause debilitating adverse consequences for patients including diabetes, cardiovascular disease and osteoporosis and contributes to irreversible organ damage. To date, there is no alternative treatment which can replicate the rapid effects of GC across multiple immune cell functions, effecting disease control during disease flares. Research efforts have focused on finding alternatives to GC, which display similar immunoregulatory actions, without the devastating adverse metabolic effects. One potential candidate is the glucocorticoid-induced leucine zipper (GILZ). GILZ is induced by low concentrations of GC and is shown to mimic the action of GC in several inflammatory processes, reducing immunity and inflammation in
MeSH term(s)	Animals ; Glucocorticoids/metabolism ; Humans ; Inflammation/metabolism ; Leucine Zippers/physiology ; Lupus Erythematosus, Systemic/metabolism ; Signal Transduction/physiology
Chemical Substances	Glucocorticoids
Language	English
Publishing date	2019-07-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01684
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Article ; Online: The heterogeneous human memory CCR6+ T helper-17 populations differ in T-bet and cytokine expression but all activate synovial fibroblasts in an IFNγ-independent manner.

Dankers, Wendy / den Braanker, Hannah / Paulissen, Sandra M J / van Hamburg, Jan Piet / Davelaar, Nadine / Colin, Edgar M / Lubberts, Erik

Arthritis research & therapy

2021 Volume 23, Issue 1, Page(s) 157

Abstract: Background: Chronic synovial inflammation is an important hallmark of inflammatory arthritis, but the cells and mechanisms involved are incompletely understood. Previously, we have shown that CCR6+ memory T-helper (memTh) cells and synovial fibroblasts ( ...

Abstract	Background: Chronic synovial inflammation is an important hallmark of inflammatory arthritis, but the cells and mechanisms involved are incompletely understood. Previously, we have shown that CCR6+ memory T-helper (memTh) cells and synovial fibroblasts (SF) activate each other in a pro-inflammatory feedforward loop, which potentially drives persistent synovial inflammation in inflammatory arthritis. However, the CCR6+ memTh cells are a heterogeneous population, containing Th17/Th22 and Th17.1 cells. Currently, it is unclear which of these subpopulations drive SF activation and how they should be targeted. In this study, we examined the individual contribution of these CCR6+ memTh subpopulations to SF activation and examined ways to regulate their function. Methods: Th17/Th22 (CXCR3 Results: Th17/Th22, Th17.1, DP, and DN cells equally express RORC but differ in production of TBX21 and cytokines like IL-17A and IFNγ. Despite these differences, all the individual CCR6+ memTh subpopulations, both from healthy individuals and RA patients, were more potent in activating SF than the classical Th1 cells. SF activation was partially inhibited by blocking IL-17A, but not by inhibiting IFNγ or TBX21. However, active vitamin D inhibited the pathogenicity of all subpopulations leading to suppression of SF activation. Conclusions: Human CCR6+ memTh cells contain several subpopulations that equally express RORC but differ in TBX21, IFNγ, and IL-17A expression. All individual Th17 subpopulations are more potent in activating SF than classical Th1 cells in an IFNγ-independent manner. Furthermore, our data suggest that IL-17A is not dominant in this T cell-SF activation loop but that a multiple T cell cytokine inhibitor, such as 1,25(OH)
MeSH term(s)	Cytokines ; Fibroblasts ; Humans ; Leukocytes, Mononuclear ; Receptors, CCR6 ; Th17 Cells
Chemical Substances	CCR6 protein, human ; Cytokines ; Receptors, CCR6
Language	English
Publishing date	2021-06-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-021-02532-9
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Article ; Online: GILZ regulates type I interferon release and sequesters STAT1.

Nataraja, Champa / Flynn, Jacqueline / Dankers, Wendy / Northcott, Melissa / Zhu, Wendy / Sherlock, Rochelle / Bennett, Taylah J / Russ, Brendan E / Miceli, Iolanda / Pervin, Mehnaz / D'Cruz, Akshay / Harris, James / Morand, Eric F / Jones, Sarah A

Journal of autoimmunity

2022 Volume 131, Page(s) 102858

Abstract: Glucocorticoids remain a mainstay of modern medicine due to their ability to broadly suppress immune activation. However, they cause severe adverse effects that warrant urgent development of a safer alternative. The glucocorticoid-induced leucine zipper ( ...

Abstract	Glucocorticoids remain a mainstay of modern medicine due to their ability to broadly suppress immune activation. However, they cause severe adverse effects that warrant urgent development of a safer alternative. The glucocorticoid-induced leucine zipper (GILZ) gene, TSC22D3, is one of the most highly upregulated genes in response to glucocorticoid treatment, and reduced GILZ mRNA and protein levels are associated with increased severity of inflammation in systemic lupus erythematosus (SLE), Ulcerative Colitis, Psoriasis, and other autoimmune/autoinflammatory diseases. Here, we demonstrate that low GILZ permits expression of a type I interferon (IFN) signature, which is exacerbated in response to TLR7 and TLR9 stimulation. Conversely, overexpression of GILZ prevents IFN-stimulated gene (ISG) up-regulation in response to IFNα. Moreover, GILZ directly binds STAT1 and prevents its nuclear translocation, thereby negatively regulating IFN-induced gene expression and the auto-amplification loop of the IFN response. Thus, GILZ powerfully regulates both the expression and action of type I IFN, suggesting restoration of GILZ as an attractive therapeutic strategy for reducing reliance on glucocorticoids.
MeSH term(s)	Gene Expression Regulation ; Glucocorticoids/metabolism ; Glucocorticoids/pharmacology ; Glucocorticoids/therapeutic use ; Humans ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Psoriasis ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism
Chemical Substances	Glucocorticoids ; Interferon Type I ; STAT1 Transcription Factor ; STAT1 protein, human
Language	English
Publishing date	2022-07-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2022.102858
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Article ; Online: Investigating immunoregulatory effects of myeloid cell autophagy in acute and chronic inflammation.

Hasnat, Md Abul / Cheang, IanIan / Dankers, Wendy / Lee, Jacinta Pw / Truong, Lynda M / Pervin, Mehnaz / Jones, Sarah A / Morand, Eric F / Ooi, Joshua D / Harris, James

Immunology and cell biology

2022 Volume 100, Issue 8, Page(s) 605–623

Abstract: Studies have highlighted a critical role for autophagy in the regulation of multiple cytokines. Autophagy inhibits the release of interleukin (IL)-1 family cytokines, including IL-1α, IL-1β and IL-18, by myeloid cells. This, in turn, impacts the release ... ...

Abstract	Studies have highlighted a critical role for autophagy in the regulation of multiple cytokines. Autophagy inhibits the release of interleukin (IL)-1 family cytokines, including IL-1α, IL-1β and IL-18, by myeloid cells. This, in turn, impacts the release of other cytokines by myeloid cells, as well as other cells of the immune system, including IL-22, IL-23, IL-17 and interferon-γ. Here, we assessed the impact of genetic depletion of the autophagy gene Atg7 in myeloid cells on acute and chronic inflammation. In a model of acute lipopolysaccharide-induced endotoxemia, loss of autophagy in myeloid cells resulted in increased release of proinflammatory cytokines, both locally and systemically. By contrast, loss of Atg7 in myeloid cells in the Lyn
MeSH term(s)	Animals ; Autophagy ; Cytokines/metabolism ; Humans ; Inflammation ; Interleukin-10/genetics ; Mice ; Myeloid Cells
Chemical Substances	Cytokines ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2022-06-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/imcb.12562
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Article: Vitamin D in Autoimmunity: Molecular Mechanisms and Therapeutic Potential.

Dankers, Wendy / Colin, Edgar M / van Hamburg, Jan Piet / Lubberts, Erik

Frontiers in immunology

2016 Volume 7, Page(s) 697

Abstract: Over the last three decades, it has become clear that the role of vitamin D goes beyond the regulation of calcium homeostasis and bone health. An important extraskeletal effect of vitamin D is the modulation of the immune system. In the context of ... ...

Abstract	Over the last three decades, it has become clear that the role of vitamin D goes beyond the regulation of calcium homeostasis and bone health. An important extraskeletal effect of vitamin D is the modulation of the immune system. In the context of autoimmune diseases, this is illustrated by correlations of vitamin D status and genetic polymorphisms in the vitamin D receptor with the incidence and severity of the disease. These correlations warrant investigation into the potential use of vitamin D in the treatment of patients with autoimmune diseases. In recent years, several clinical trials have been performed to investigate the therapeutic value of vitamin D in multiple sclerosis, rheumatoid arthritis, Crohn's disease, type I diabetes, and systemic lupus erythematosus. Additionally, a second angle of investigation has focused on unraveling the molecular pathways used by vitamin D in order to find new potential therapeutic targets. This review will not only provide an overview of the clinical trials that have been performed but also discuss the current knowledge about the molecular mechanisms underlying the immunomodulatory effects of vitamin D and how these advances can be used in the treatment of autoimmune diseases.
Language	English
Publishing date	2016
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2016.00697
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Article ; Online: Human Memory Th17 Cell Populations Change Into Anti-inflammatory Cells With Regulatory Capacity Upon Exposure to Active Vitamin D.

Dankers, Wendy / Davelaar, Nadine / van Hamburg, Jan Piet / van de Peppel, Jeroen / Colin, Edgar M / Lubberts, Erik

Frontiers in immunology

2019 Volume 10, Page(s) 1504

Abstract: Autoimmune diseases are characterized by an aberrantly activated immune system, resulting in tissue damage and functional disability in patients. An important therapeutic goal is to restore the deregulated immunological balance between pro- and anti- ... ...

Abstract	Autoimmune diseases are characterized by an aberrantly activated immune system, resulting in tissue damage and functional disability in patients. An important therapeutic goal is to restore the deregulated immunological balance between pro- and anti-inflammatory T cells. This imbalance is illustrated by elevated levels and activity of memory Th17 cell populations, such as Th17, Th1/Th17, and Th17.1 cells, in various autoimmune diseases. These cells are characterized by the chemokine receptor CCR6, RORC expression and production of IL-17A, IFNγ, and TNFα. Using rheumatoid arthritis (RA) as a model of autoimmune disease, we here demonstrate that pro-inflammatory memory CCR6+ Th cells can switch into anti-inflammatory cells with regulatory capacity using the active vitamin D metabolite 1,25(OH)
MeSH term(s)	Adult ; Anti-Inflammatory Agents/immunology ; Arthritis, Rheumatoid/immunology ; Autoimmune Diseases/immunology ; CD3 Complex/immunology ; Cells, Cultured ; Female ; Humans ; Immunologic Memory/immunology ; Interleukins/immunology ; Male ; Middle Aged ; Receptors, CCR6/immunology ; Th17 Cells/immunology ; Tumor Necrosis Factor-alpha/immunology ; Vitamin D/immunology
Chemical Substances	Anti-Inflammatory Agents ; CD3 Complex ; Interleukins ; Receptors, CCR6 ; Tumor Necrosis Factor-alpha ; Vitamin D (1406-16-2)
Language	English
Publishing date	2019-07-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01504
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Article ; Online: Type 1 interferon suppresses expression and glucocorticoid induction of glucocorticoid-induced leucine zipper (GILZ).

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

Frontiers in immunology

2022 Volume 13, Page(s) 1034880

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) ... ...

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
Language	English
Publishing date	2022-11-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1034880
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Article ; Online: 1,25(OH)

Dankers, Wendy / González-Leal, Claudia / Davelaar, Nadine / Asmawidjaja, Patrick S / Mus, Adriana M C / Hazes, Johanna M W / Colin, Edgar M / Lubberts, Erik

Arthritis research & therapy

2018 Volume 20, Issue 1, Page(s) 212

Abstract: Background: Despite recent improvements in the treatment of rheumatoid arthritis (RA), an insufficient treatment response and the development of treatment resistance in many patients illustrates the need for new therapeutic strategies. Chronic synovial ... ...

Abstract	Background: Despite recent improvements in the treatment of rheumatoid arthritis (RA), an insufficient treatment response and the development of treatment resistance in many patients illustrates the need for new therapeutic strategies. Chronic synovial inflammation could be suppressed by targeting RA synovial fibroblast (RASF) activation by, for example, interleukin (IL)-17A-producing CCR6 Methods: CCR6 Results: 1,25(OH) Conclusion: This study suggests that 1,25(OH)
MeSH term(s)	Calcitriol/administration & dosage ; Coculture Techniques ; Dexamethasone/administration & dosage ; Drug Synergism ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/metabolism ; Receptors, CCR6/biosynthesis ; Synovial Membrane/drug effects ; Synovial Membrane/metabolism ; T-Lymphocytes, Helper-Inducer/drug effects ; T-Lymphocytes, Helper-Inducer/metabolism ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	CCR6 protein, human ; Receptors, CCR6 ; Tumor Necrosis Factor-alpha ; Dexamethasone (7S5I7G3JQL) ; Calcitriol (FXC9231JVH)
Language	English
Publishing date	2018-09-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-018-1706-9
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Article ; Online: Necrotic cell death increases the release of macrophage migration inhibitory factor by monocytes/macrophages.

Dankers, Wendy / Hasnat, Md Abul / Swann, Vanesa / Alharbi, Arwaf / Lee, Jacinta Pw / Cristofaro, Megan A / Gantier, Michael P / Jones, Sarah A / Morand, Eric F / Flynn, Jacqueline K / Harris, James

Immunology and cell biology

2020 Volume 98, Issue 9, Page(s) 782–790

Abstract: Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory molecule with both cytokine and noncytokine activity. MIF is constitutively released from multiple cell types via an unconventional secretory pathway that is not well defined. ... ...

Abstract	Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory molecule with both cytokine and noncytokine activity. MIF is constitutively released from multiple cell types via an unconventional secretory pathway that is not well defined. Here, we looked at MIF release from human and mouse monocytes/macrophages in response to different stimuli. While MIF release was not significantly altered in response to lipopolysaccharide or heat-killed Escherichia coli, cytotoxic stimuli strongly promoted release of MIF. MIF release was highly upregulated in cells undergoing necrosis, necroptosis and NLRP3 inflammasome-dependent pyroptosis. Our data suggest that cell death represents a major route for MIF release from myeloid cells. The functional significance of these findings and their potential importance in the context of autoimmune and inflammatory diseases warrant further investigation.
MeSH term(s)	Animals ; Cell Death ; Macrophage Migration-Inhibitory Factors/metabolism ; Macrophages/metabolism ; Mice ; Monocytes/metabolism ; Necroptosis ; Pyroptosis
Chemical Substances	Macrophage Migration-Inhibitory Factors
Language	English
Publishing date	2020-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/imcb.12376
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