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Article ; Online: The role of IL-23 receptor signaling in inflammation-mediated erosive autoimmune arthritis and bone remodeling.

Razawy, Wida / van Driel, Marjolein / Lubberts, Erik

2018 Volume 48, Issue 2, Page(s) 220–229

Abstract: The IL-23/Th17 axis has been implicated in the development of autoimmune diseases, such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). RA and PsA are heterogeneous diseases with substantial burden on patients. Increasing evidence suggests ... ...

Abstract	The IL-23/Th17 axis has been implicated in the development of autoimmune diseases, such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). RA and PsA are heterogeneous diseases with substantial burden on patients. Increasing evidence suggests that the IL-23 signaling pathway may be involved in the development of autoimmunity and erosive joint damage. IL-23 can act either directly or indirectly on bone forming osteoblasts as well as on bone resorbing osteoclasts. As IL-23 regulates the activity of cells of the bone, it is conceivable that in addition to inflammation-mediated joint erosion, IL-23 may play a role in physiological bone remodeling. In this review, we focus on the role of IL-23 in autoimmune arthritis in patients and murine models, and provide an overview of IL-23 producing and responding cells in autoimmune arthritic joints. In addition, we discuss the role of IL-23 on bone forming osteoblasts and bone resorbing osteoclasts regarding inflammation-mediated joint damage and bone remodeling. At last, we briefly discuss the clinical implications of targeting this pathway for joint damage and systemic bone loss in autoimmune arthritis.
MeSH term(s)	Animals ; Arthritis, Psoriatic/immunology ; Arthritis, Rheumatoid/immunology ; Autoimmunity ; Bone Resorption ; Disease Models, Animal ; Humans ; Inflammation/immunology ; Interleukin-23/immunology ; Mice ; Osteoclasts/immunology ; Signal Transduction
Chemical Substances	Interleukin-23
Language	English
Publishing date	2018-01-15
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201646787
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Characterizing memory T helper cells in patients with psoriasis, subclinical, or early psoriatic arthritis using a machine learning algorithm.

den Braanker, Hannah / Razawy, Wida / Wervers, Kim / Mus, Anne-Marie C / Davelaar, Nadine / Kok, Marc R / Lubberts, Erik

Arthritis research & therapy

2022 Volume 24, Issue 1, Page(s) 28

Abstract: Background: Psoriasis patients developing psoriatic arthritis (PsA) are thought to go through different phases. Understanding the underlying events in these phases is crucial to diagnose PsA early. Here, we have characterized the circulating memory T ... ...

Abstract	Background: Psoriasis patients developing psoriatic arthritis (PsA) are thought to go through different phases. Understanding the underlying events in these phases is crucial to diagnose PsA early. Here, we have characterized the circulating memory T helper (Th) cells in psoriasis patients with or without arthralgia, psoriasis patients who developed PsA during follow-up (subclinical PsA), early PsA patients and healthy controls to elucidate their role in PsA development. Methods: We used peripheral blood mononuclear cells of sex and age-matched psoriasis patients included in Rotterdam Joint Skin study (n=22), early PsA patients included in Dutch South West Early Psoriatic Arthritis Cohort (DEPAR) (n=23) and healthy controls (HC; n=17). We profiled memory Th cell subsets with flow cytometry and used the machine learning algorithm FlowSOM to interpret the data. Results: Three of the 22 psoriasis patients developed PsA during 2-year follow-up. FlowSOM identified 12 clusters of memory Th cells, including Th1, Th2, Th17/22, and Th17.1 cells. All psoriasis and PsA patients had higher numbers of Th17/22 than healthy controls. Psoriasis patients without arthralgia had lower numbers of CCR6 Conclusions: Unsupervised clustering analysis revealed differences in circulating memory Th cells between psoriasis and PsA patients compared to HC; however, no specific subset was identified characterizing subclinical PsA patients.
MeSH term(s)	Arthritis, Psoriatic/diagnosis ; Humans ; Leukocytes, Mononuclear ; Machine Learning ; Psoriasis/diagnosis ; Th17 Cells
Language	English
Publishing date	2022-01-19
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/s13075-021-02714-5
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Article ; Online: CD4

Razawy, Wida / Asmawidjaja, Patrick S / Mus, Anne-Marie / Salioska, Nazike / Davelaar, Nadine / Kops, Nicole / Oukka, Mohamed / Alves, C Henrique / Lubberts, Erik

European journal of immunology

2019 Volume 50, Issue 2, Page(s) 245–255

Abstract: IL-23 plays an important role in the development of arthritis and the IL-23 receptor (IL-23R) is expressed on different types of T cells. However, it is not fully clear which IL- ... ...

Abstract	IL-23 plays an important role in the development of arthritis and the IL-23 receptor (IL-23R) is expressed on different types of T cells. However, it is not fully clear which IL-23R
MeSH term(s)	Adoptive Transfer/methods ; Animals ; Arthritis/immunology ; CD4-Positive T-Lymphocytes/immunology ; Disease Models, Animal ; Female ; Inflammation/immunology ; Interleukin-17/immunology ; Interleukin-23/immunology ; Lymphoid Tissue/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, CCR6/immunology ; Receptors, Interleukin/immunology ; Th17 Cells/immunology
Chemical Substances	CCR6 protein, mouse ; Interleukin-17 ; Interleukin-23 ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, CCR6 ; Receptors, Interleukin ; interleukin-23 receptor, mouse
Language	English
Publishing date	2019-11-28
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201948112
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation.

Razawy, Wida / Alves, Celso H / Koedam, Marijke / Asmawidjaja, Patrick S / Mus, Adriana M C / Oukka, Mohamed / Leenen, Pieter J M / Visser, Jenny A / van der Eerden, Bram C J / Lubberts, Erik

Scientific reports

2021 Volume 11, Issue 1, Page(s) 10244

Abstract: The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the ... ...

Abstract	The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the regulation of bone homeostasis remains elusive. Therefore, we studied the role of IL-23R signaling in physiological bone remodeling using IL-23R deficient mice. Using µCT, we demonstrate that 7-week-old IL-23R
MeSH term(s)	Animals ; Bone Density ; Bone Development ; Bone Remodeling ; Bone and Bones/metabolism ; Bone and Bones/physiology ; Cell Differentiation ; Cells, Cultured ; Female ; Femur/metabolism ; Gene Knock-In Techniques/methods ; Interleukin-23/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Osteogenesis/genetics ; Osteogenesis/physiology ; Receptors, Interleukin/deficiency ; Receptors, Interleukin/genetics ; Receptors, Interleukin/metabolism
Chemical Substances	Interleukin-23 ; Receptors, Interleukin ; interleukin-23 receptor, mouse
Language	English
Publishing date	2021-05-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-89625-2
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Article ; Online: Treatment of primary plasma cell leukaemia with carfilzomib and lenalidomide-based therapy (EMN12/HOVON-129): final analysis of a non-randomised, multicentre, phase 2 study.

van de Donk, Niels W C J / Minnema, Monique C / van der Holt, Bronno / Schjesvold, Fredrik / Wu, Ka Lung / Broijl, Annemiek / Roeloffzen, Wilfried W H / Gadisseur, Alain / Pietrantuono, Giuseppe / Pour, Ludek / van der Velden, Vincent H J / Lund, Thomas / Offidani, Massimo / Grasso, Mariella / Giaccone, Luisa / Razawy, Wida / Tacchetti, Paola / Mancuso, Katia / Silkjaer, Trine /

Caers, Jo / Zweegman, Sonja / Hájek, Roman / Benjamin, Reuben / Vangsted, Annette Juul / Boccadoro, Mario / Gay, Francesca / Sonneveld, Pieter / Musto, Pellegrino

The Lancet. Oncology

2023 Volume 24, Issue 10, Page(s) 1119–1133

Abstract: Background: Primary plasma cell leukaemia is a rare and aggressive plasma cell disorder with a poor prognosis. The aim of the EMN12/HOVON-129 study was to improve the outcomes of patients with primary plasma cell leukaemia by incorporating carfilzomib ... ...

Abstract	Background: Primary plasma cell leukaemia is a rare and aggressive plasma cell disorder with a poor prognosis. The aim of the EMN12/HOVON-129 study was to improve the outcomes of patients with primary plasma cell leukaemia by incorporating carfilzomib and lenalidomide in induction, consolidation, and maintenance therapy. Methods: The EMN12/HOVON-129 study is a non-randomised, phase 2, multicentre study conducted at 19 academic centres and hospitals in seven European countries (Belgium, Czech Republic, Denmark, Italy, Norway, The Netherlands, and the UK) for previously untreated patients with primary plasma cell leukaemia aged 18 years or older. Inclusion criteria were newly diagnosed primary plasma cell leukaemia (defined as >2 ×10 Findings: Between Oct 23, 2015, and Aug 5, 2021, 61 patients were enrolled and received KRd induction treatment (36 patients aged 18-65 years [20 (56%) were male and 16 (44%) female], and 25 aged ≥66 years [12 (48%) were male and 13 (52%) female]). With a median follow-up of 43·5 months (IQR 27·7-67·8), the median progression-free survival was 15·5 months (95% CI 9·4-38·4) for younger patients. For older patients, median follow-up was 32·0 months (IQR 24·7-34·6), and median progression-free survival was 13·8 months (95% CI 9·2-35·5). Adverse events were most frequently observed directly after treatment initiation, with infections (two of 36 (6%) younger patients and eight of 25 (32%) older patients) and respiratory events (two of 36 [6%] younger patients and four of 25 [16%] older patients) being the most common grade 3 or greater events during the first four KRd cycles. Treatment-related serious adverse events were reported in 26 (72%) of 36 younger patients and in 19 (76%) of 25 older patients, with infections being the most common. Treatment-related deaths were reported in none of the younger patients and three (12%) of the older patients (two infections and one unknown cause of death). Interpretation: Carfilzomib and lenalidomide-based therapy provides improved progression-free survival compared with previously published data. However, results remain inferior in primary plasma cell leukaemia compared with multiple myeloma, highlighting the need for new studies incorporating novel immunotherapies. Funding: Dutch Cancer Society, Celgene (a BMS company), and AMGEN.
Language	English
Publishing date	2023-09-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2049730-1
ISSN	1474-5488 ; 1470-2045
ISSN (online)	1474-5488
ISSN	1470-2045
DOI	10.1016/S1470-2045(23)00405-9
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Zs.A 5696: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Dendritic Cell-Specific Deletion of β-Catenin Results in Fewer Regulatory T-Cells without Exacerbating Autoimmune Collagen-Induced Arthritis.

Alves, C Henrique / Ober-Blöbaum, Julia L / Brouwers-Haspels, Inge / Asmawidjaja, Patrick S / Mus, Adriana M C / Razawy, Wida / Molendijk, Marlieke / Clausen, Björn E / Lubberts, Erik

PloS one

2015 Volume 10, Issue 11, Page(s) e0142972

Abstract: Dendritic cells (DCs) are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating tolerogenic DC function in vivo remain largely unknown. The β-catenin ... ...

Abstract	Dendritic cells (DCs) are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating tolerogenic DC function in vivo remain largely unknown. The β-catenin pathway has been suggested to promote a regulatory DC phenotype. The aim of this study was to unravel the role of β-catenin signalling to control DC function in the autoimmune collagen-induced arthritis model (CIA). Deletion of β-catenin specifically in DCs was achieved by crossing conditional knockout mice with a CD11c-Cre transgenic mouse line. Bone marrow-derived DCs (BMDCs) were generated and used to study the maturation profile of these cells in response to a TLR2 or TLR4 ligand stimulation. CIA was induced by intra-dermal immunization with 100 μg chicken type II collagen in complete Freund's adjuvant on days 0 and 21. CIA incidence and severity was monitored macroscopically and by histology. The T cell profile as well as their cytokine production were analysed by flow cytometry. Lack of β-catenin specifically in DCs did not affect the spontaneous, TLR2- or TLR4-induced maturation and activation of BMDCs or their cytokine production. Moreover, no effect on the incidence and severity of CIA was observed in mice lacking β-catenin in CD11c+ cells. A decreased frequency of splenic CD3+CD8+ T cells and of regulatory T cells (Tregs) (CD4+CD25highFoxP3+), but no changes in the frequency of splenic Th17 (CCR6+CXCR3-CCR4+), Th2 (CCR6-CXCR3-CCR4+) and Th1 (CCR6-CXCR3+CCR4-) cells were observed in these mice under CIA condition. Furthermore, the expression of IL-17A, IL-17F, IL-22, IL-4 or IFNγ was also not affected. Our data indicate that ablation of β-catenin expression in DCs did not alter the course and severity of CIA. We conclude that although deletion of β-catenin resulted in a lower frequency of Tregs, this decrease was not sufficient to aggravate the onset and severity of CIA.
MeSH term(s)	Animals ; Antigen-Presenting Cells/immunology ; Antigen-Presenting Cells/metabolism ; Arthritis, Experimental/genetics ; Arthritis, Experimental/immunology ; Arthritis, Experimental/pathology ; Collagen Type II/administration & dosage ; Collagen Type II/immunology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Humans ; Immune Tolerance ; Mice ; Mice, Knockout ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Toll-Like Receptor 2/immunology ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 4/immunology ; Toll-Like Receptor 4/metabolism ; beta Catenin/biosynthesis ; beta Catenin/genetics
Chemical Substances	Collagen Type II ; Tlr2 protein, mouse ; Tlr4 protein, mouse ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; beta Catenin
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0142972
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Article ; Online: Inhibition of MicroRNA-494 Reduces Carotid Artery Atherosclerotic Lesion Development and Increases Plaque Stability.

Wezel, Anouk / Welten, Sabine M J / Razawy, Wida / Lagraauw, H Maxime / de Vries, Margreet R / Goossens, Eveline A C / Boonstra, Martin C / Hamming, Jaap F / Kandimalla, Ekambar R / Kuiper, Johan / Quax, Paul H A / Nossent, A Yaël / Bot, Ilze

Annals of surgery

2015 Volume 262, Issue 5, Page(s) 841–7; discussion 847–8

Abstract: Objectives: Unstable atherosclerotic lesions in carotid arteries require surgical endarterectomy to reduce the risk of ischemic stroke. We aimed to identify microRNAs that exert a broad effect on atherosclerotic plaque formation and stability in the ... ...

Abstract	Objectives: Unstable atherosclerotic lesions in carotid arteries require surgical endarterectomy to reduce the risk of ischemic stroke. We aimed to identify microRNAs that exert a broad effect on atherosclerotic plaque formation and stability in the carotid artery. Background: We made a selection of 164 genes involved in atherosclerosis. Using www.targetscan.org, we determined which microRNAs potentially regulate expression of these genes. We identified multiple microRNAs from the 14q32 microRNA cluster, which is highly involved in vascular remodeling. In human plaques, collected during carotid endarterectomy surgery, we found that 14q32 microRNA (miR-494) was abundantly expressed in unstable lesions. Methods: We induced atherosclerotic plaque formation in hypercholesterolemic ApoE mice by placing semiconstrictive collars around both carotid arteries. We injected "Gene Silencing Oligonucleotides" against miR-494 (GSO-494) or negative control (GSO-control). Using fluorescently labeled GSOs, we confirmed uptake of GSOs in affected areas of the carotids, but not elsewhere in the vasculature. Results: After injection of GSO-494, we observed significant downregulation of miR-494 expression in the carotid arteries, although miR-494 target genes were upregulated. Further analyses revealed a 65% decrease in plaque size after GSO-494 treatment. Plaque stability was increased in GSO-494-treated mice, determined by an 80% decrease in necrotic core size and a 50% increase in plaque collagen content. Inhibition of miR-494 also resulted in decreased cholesterol levels and decreased very low-density lipoprotein (VLDL) fractions. Conclusions: Treatment with GSO-494 results in smaller atherosclerotic lesions with increased plaque stability. Inhibition of miR-494 may decrease the risk of surgical complications or even avert endarterectomy surgery in some cases.
MeSH term(s)	Animals ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Blotting, Western ; Carotid Arteries ; DNA/genetics ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Male ; Mice ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; Plaque, Atherosclerotic/genetics ; Plaque, Atherosclerotic/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	MicroRNAs ; Mirn494 microRNA, mouse ; DNA (9007-49-2)
Language	English
Publishing date	2015-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	340-2
ISSN	1528-1140 ; 0003-4932
ISSN (online)	1528-1140
ISSN	0003-4932
DOI	10.1097/SLA.0000000000001466
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Article ; Online: The role of IL-23 receptor signaling in inflammation-mediated erosive autoimmune arthritis and bone remodeling.

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Article ; Online: Characterizing memory T helper cells in patients with psoriasis, subclinical, or early psoriatic arthritis using a machine learning algorithm.

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Article ; Online: CD4

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Article ; Online: IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation.

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Article ; Online: Treatment of primary plasma cell leukaemia with carfilzomib and lenalidomide-based therapy (EMN12/HOVON-129): final analysis of a non-randomised, multicentre, phase 2 study.

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Article ; Online: Dendritic Cell-Specific Deletion of β-Catenin Results in Fewer Regulatory T-Cells without Exacerbating Autoimmune Collagen-Induced Arthritis.

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Article ; Online: Inhibition of MicroRNA-494 Reduces Carotid Artery Atherosclerotic Lesion Development and Increases Plaque Stability.

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