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Article: Therapeutic Options for Systemic Sclerosis: Current and Future Perspectives in Tackling Immune-Mediated Fibrosis.

Papadimitriou, Theodoros-Ioannis / van Caam, Arjan / van der Kraan, Peter M / Thurlings, Rogier M

2022 Volume 10, Issue 2

Abstract: Systemic sclerosis (SSc) is a severe auto-immune, rheumatic disease, characterized by excessive fibrosis of the skin and visceral organs. SSc is accompanied by high morbidity and mortality rates, and unfortunately, few disease-modifying therapies are ... ...

Abstract	Systemic sclerosis (SSc) is a severe auto-immune, rheumatic disease, characterized by excessive fibrosis of the skin and visceral organs. SSc is accompanied by high morbidity and mortality rates, and unfortunately, few disease-modifying therapies are currently available. Inflammation, vasculopathy, and fibrosis are the key hallmarks of SSc pathology. In this narrative review, we examine the relationship between inflammation and fibrosis and provide an overview of the efficacy of current and novel treatment options in diminishing SSc-related fibrosis based on selected clinical trials. To do this, we first discuss inflammatory pathways of both the innate and acquired immune systems that are associated with SSc pathophysiology. Secondly, we review evidence supporting the use of first-line therapies in SSc patients. In addition, T cell-, B cell-, and cytokine-specific treatments that have been utilized in SSc are explored. Finally, the potential effectiveness of tyrosine kinase inhibitors and other novel therapeutic approaches in reducing fibrosis is highlighted.
Language	English
Publishing date	2022-01-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10020316
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Article ; Online: Growth factors that drive aggrecan synthesis in healthy articular cartilage. Role for transforming growth factor-β?

van der Kraan, Peter M / van Caam, Arjan P M / Blaney Davidson, Esmeralda N / van den Bosch, Martijn H J / van de Loo, Fons A J

Osteoarthritis and cartilage open

2024 Volume 6, Issue 2, Page(s) 100459

Abstract: Introduction: Articular cartilage makes smooth movement possible and destruction of this tissue leads to loss of joint function. An important biomolecule that determines this function is the large aggregating proteoglycan of cartilage, aggrecan. ... ...

Abstract	Introduction: Articular cartilage makes smooth movement possible and destruction of this tissue leads to loss of joint function. An important biomolecule that determines this function is the large aggregating proteoglycan of cartilage, aggrecan. Aggrecan has a relatively short half-life in cartilage and therefore continuous production of this molecule is essential. Methods: In this narrative review we discuss what is the role of growth factors in driving the synthesis of aggrecan in articular cartilage. A literature search has been done using the search items; cartilage, aggrecan, explant, Transforming Growth factor-β (TGF-β), Insulin-like Growth Factor (IGF), Bone Morphogenetic Protein (BMP) and the generic term "growth factors". Focus has been on studies using healthy cartilage and models of cartilage regeneration have been excluded. Results: In healthy adult articular cartilage IGF is the main factor that drives aggrecan synthesis and maintains adequate levels of production. BMP's and TGF-β have a very limited role but appear to be more important during chondrogenesis and cartilage development. The major role of TGF-β is not stimulation of aggrecan synthesis but maintenance of the differentiated articular cartilage chondrocyte phenotype. Conclusion: TGF-β is a factor that is generally considered as an important factor in stimulating aggrecan synthesis in cartilage but its role in this might be very restrained in healthy, adult articular cartilage.
Language	English
Publishing date	2024-03-07
Publishing country	England
Document type	Journal Article ; Review
ISSN	2665-9131
ISSN (online)	2665-9131
DOI	10.1016/j.ocarto.2024.100459
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Article ; Online: Systemic sclerosis-associated pulmonary arterial hypertension is characterized by a distinct peripheral T helper cell profile.

Papadimitriou, Theodoros-Ioannis / Lemmers, Jacqueline M J / van Caam, Arjan P M / Vos, Jacqueline / Vitters, Elly / Stinessen, Lizan / van Leuven, Sander I / Koenders, Marije / van der Kraan, Peter M / Koenen, Hans J P M / Smeets, Ruben / Nijveldt, Robin / Vonk, Madelon C / Thurlings, R M

Rheumatology (Oxford, England)

2024

Abstract: Objectives: Systemic sclerosis (SSc) is characterized by multiple clinical manifestations. Vasculopathy is a main disease hallmark and ranges in severity from an exacerbated Raynaud phenomenon to pulmonary arterial hypertension (PAH). The potential ... ...

Abstract	Objectives: Systemic sclerosis (SSc) is characterized by multiple clinical manifestations. Vasculopathy is a main disease hallmark and ranges in severity from an exacerbated Raynaud phenomenon to pulmonary arterial hypertension (PAH). The potential involvement of immune system in SSc associated vascular abnormalities is not clear. Here, we set out to study SSc-related immune parameters and determine whether and which peripheral T cell subsets associate with vascular severity in SSc patients. Methods: Peripheral blood and clinical data were collected from 30 SSc patients, 5 patients with idiopathic pulmonary arterial hypertension (IPAH) and 15 age and sex-matched healthy donors (HD). In this cross-sectional cohort SSc patients with PAH (n = 15) were matched for their age, sex and medication with SSc patients with no signs of PAH (n = 15). Lymphocyte subsets were quantified by multi-colour flow cytometry. Results: SSc patients exhibited elevated percentages of T peripheral helper cells (Tph), CD4+GZMB+ T cells and decreased levels of Th1 cells compared with HD. Increased presence of both CD4+ and CD8+ exhausted-like (CD28-) T cells, characterized by raised cytokine and cytotoxic signature, was also observed in SSc compared with HD blood. Furthermore, IL-4 expressing CD4+CD8+ T cells were significantly increased in SSc peripheral blood. Interestingly, the presence of PAH in SSc was accompanied by a distinct T helper profile, characterized by raised percentages of Th17 and Tph cells. Conclusion: SSc patients with severe vasculopathy (presence of PAH) exhibited a distinct T cell profile, suggesting for a potential role of auto-immune inflammation in SSc vascular complications.
Language	English
Publishing date	2024-03-29
Publishing country	England
Document type	Journal Article
ZDB-ID	1464822-2
ISSN	1462-0332 ; 1462-0324
ISSN (online)	1462-0332
ISSN	1462-0324
DOI	10.1093/rheumatology/keae190
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Article ; Online: Therapeutic Options for Systemic Sclerosis

Theodoros-Ioannis Papadimitriou / Arjan van Caam / Peter M. van der Kraan / Rogier M. Thurlings

Biomedicines, Vol 10, Iss 316, p

Current and Future Perspectives in Tackling Immune-Mediated Fibrosis

2022 Volume 316

Abstract	Systemic sclerosis (SSc) is a severe auto-immune, rheumatic disease, characterized by excessive fibrosis of the skin and visceral organs. SSc is accompanied by high morbidity and mortality rates, and unfortunately, few disease-modifying therapies are currently available. Inflammation, vasculopathy, and fibrosis are the key hallmarks of SSc pathology. In this narrative review, we examine the relationship between inflammation and fibrosis and provide an overview of the efficacy of current and novel treatment options in diminishing SSc-related fibrosis based on selected clinical trials. To do this, we first discuss inflammatory pathways of both the innate and acquired immune systems that are associated with SSc pathophysiology. Secondly, we review evidence supporting the use of first-line therapies in SSc patients. In addition, T cell-, B cell-, and cytokine-specific treatments that have been utilized in SSc are explored. Finally, the potential effectiveness of tyrosine kinase inhibitors and other novel therapeutic approaches in reducing fibrosis is highlighted.
Keywords	systemic sclerosis ; immune cells ; anti-inflammatory ; therapy ; fibrosis ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: TGF-β is elevated in hyperuricemic individuals and mediates urate-induced hyperinflammatory phenotype in human mononuclear cells.

Klück, Viola / Cabău, Georgiana / Mies, Linda / Bukkems, Femke / van Emst, Liesbeth / Bakker, René / van Caam, Arjan / Crişan, Tania O / Joosten, Leo A B

Arthritis research & therapy

2023 Volume 25, Issue 1, Page(s) 30

Abstract: Background: Soluble urate leads to a pro-inflammatory phenotype in human monocytes characterized by increased production of IL-1β and downregulation of IL-1 receptor antagonist, the mechanism of which remains to be fully elucidated. Previous ... ...

Abstract	Background: Soluble urate leads to a pro-inflammatory phenotype in human monocytes characterized by increased production of IL-1β and downregulation of IL-1 receptor antagonist, the mechanism of which remains to be fully elucidated. Previous transcriptomic data identified differential expression of genes in the transforming growth factor (TGF)-β pathway in monocytes exposed to urate in vitro. In this study, we explore the role of TGF-β in urate-induced hyperinflammation in peripheral blood mononuclear cells (PBMCs). Methods: TGF-β mRNA in unstimulated PBMCs and protein levels in plasma were measured in individuals with normouricemia, hyperuricemia and gout. For in vitro validation, PBMCs of healthy volunteers were isolated and treated with a dose ranging concentration of urate for assessment of mRNA and pSMAD2. Urate and TGF-β priming experiments were performed with three inhibitors of TGF-β signalling: SB-505124, 5Z-7-oxozeaenol and a blocking antibody against TGF-β receptor II. Results: TGF-β mRNA levels were elevated in gout patients compared to healthy controls. TGF-β-LAP levels in serum were significantly higher in individuals with hyperuricemia compared to controls. In both cases, TGF-β correlated positively to serum urate levels. In vitro, urate exposure of PBMCs did not directly induce TGF-β but did enhance SMAD2 phosphorylation. The urate-induced pro-inflammatory phenotype of monocytes was partly reversed by blocking TGF-β. Conclusions: TGF-β is elevated in individuals with hyperuricemia and correlated to serum urate concentrations. In addition, the urate-induced pro-inflammatory phenotype in human monocytes is mediated by TGF-β signalling. Future studies are warranted to explore the intracellular pathways involved and to assess the clinical significance of urate-TGF-β relation.
MeSH term(s)	Humans ; Gout/genetics ; Hyperuricemia ; Leukocytes ; Leukocytes, Mononuclear ; Uric Acid/pharmacology ; Transforming Growth Factor beta/genetics
Chemical Substances	Uric Acid (268B43MJ25) ; Transforming Growth Factor beta
Language	English
Publishing date	2023-02-27
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/s13075-023-03001-1
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Article ; Online: CD7 activation regulates cytotoxicity-driven pathology in systemic sclerosis, yielding a target for selective cell depletion.

Papadimitriou, Theodoros Ioannis / Singh, Prashant / van Caam, Arjan / Walgreen, Birgitte / Gorris, Mark A J / Vitters, Elly L / van Ingen, Iris L / Koenders, Marije I / Smeets, Ruben L / Vonk, Madelon / de Vries, Jolanda M / van der Kraan, Peter M / van Oosterhout, Ypke / Huynen, Martijn A / Koenen, Hans J P M / Thurlings, Rogier M

Annals of the rheumatic diseases

2024 Volume 83, Issue 4, Page(s) 488–498

Abstract: Objectives: Cytotoxic T cells and natural killer (NK) cells are central effector cells in cancer and infections. Their effector response is regulated by activating and inhibitory receptors. The regulation of these cells in systemic autoimmune diseases ... ...

Abstract	Objectives: Cytotoxic T cells and natural killer (NK) cells are central effector cells in cancer and infections. Their effector response is regulated by activating and inhibitory receptors. The regulation of these cells in systemic autoimmune diseases such as systemic sclerosis (SSc) is less defined. Methods: We conducted ex vivo analysis of affected skin and blood samples from 4 SSc patient cohorts (a total of 165 SSc vs 80 healthy individuals) using single-cell transcriptomics, flow cytometry and multiplex immunofluorescence staining. We further analysed the effects of costimulatory modulation in functional assays, and in a severely affected SSc patient who was treated on compassionate use with a novel anti-CD3/CD7 immunotoxin treatment. Results: Here, we show that SSc-affected skin contains elevated numbers of proliferating T cells, cytotoxic T cells and NK cells. These cells selectively express the costimulatory molecule CD7 in association with cytotoxic, proinflammatory and profibrotic genes, especially in recent-onset and severe disease. We demonstrate that CD7 regulates the cytolytic activity of T cells and NK cells and that selective depletion of CD7 Conclusion: Together, the findings imply costimulatory molecules as key regulators of cytotoxicity-driven pathology in systemic autoimmune disease, yielding CD7 as a novel target for selective depletion of pathogenic cells.
MeSH term(s)	Humans ; Antigens, CD7/metabolism ; Killer Cells, Natural ; Scleroderma, Systemic ; T-Lymphocytes
Chemical Substances	Antigens, CD7
Language	English
Publishing date	2024-03-12
Publishing country	England
Document type	Journal Article
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/ard-2023-224827
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Article: Transcription Factors in Cartilage Homeostasis and Osteoarthritis.

Neefjes, Margot / van Caam, Arjan P M / van der Kraan, Peter M

Biology

2020 Volume 9, Issue 9

Abstract: Osteoarthritis (OA) is the most common degenerative joint disease, and it is characterized by articular cartilage loss. In part, OA is caused by aberrant anabolic and catabolic activities of the chondrocyte, the only cell type present in cartilage. These ...

Abstract	Osteoarthritis (OA) is the most common degenerative joint disease, and it is characterized by articular cartilage loss. In part, OA is caused by aberrant anabolic and catabolic activities of the chondrocyte, the only cell type present in cartilage. These chondrocyte activities depend on the intra- and extracellular signals that the cell receives and integrates into gene expression. The key proteins for this integration are transcription factors. A large number of transcription factors exist, and a better understanding of the transcription factors activated by the various signaling pathways active during OA can help us to better understand the complex etiology of OA. In addition, establishing such a profile can help to stratify patients in different subtypes, which can be a very useful approach towards personalized therapy. In this review, we discuss crucial transcription factors for extracellular matrix metabolism, chondrocyte hypertrophy, chondrocyte senescence, and autophagy in chondrocytes. In addition, we discuss how insight into these factors can be used for treatment purposes.
Language	English
Publishing date	2020-09-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology9090290
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Article ; Online: Nailfold capillaroscopy and candidate-biomarker levels in systemic sclerosis-associated pulmonary hypertension: A cross-sectional study.

Lemmers, Jacqueline Mj / van Caam, Arjan Pm / Kersten, Brigit / van den Ende, Cornelia Hm / Knaapen, Hanneke / van Dijk, Arie Pj / Hagmolen Of Ten Have, Wanda / van den Hoogen, Frank Hj / Koenen, Hans / van Leuven, Sander I / Alkema, Wynand / Smeets, Ruben L / Vonk, Madelon C

Journal of scleroderma and related disorders

2023 Volume 8, Issue 3, Page(s) 221–230

Abstract: Objectives: Pulmonary hypertension is one of the leading causes of death in systemic sclerosis. Early detection and treatment of pulmonary hypertension in systemic sclerosis is crucial. Nailfold capillaroscopy microscopy, vascular autoantibodies AT1R ... ...

Abstract	Objectives: Pulmonary hypertension is one of the leading causes of death in systemic sclerosis. Early detection and treatment of pulmonary hypertension in systemic sclerosis is crucial. Nailfold capillaroscopy microscopy, vascular autoantibodies AT1R and ETAR, and several candidate-biomarkers have the potential to serve as noninvasive tools to identify systemic sclerosis patients at risk for developing pulmonary hypertension. Here, we explore the classifying potential of nailfold capillaroscopy microscopy characteristics and serum levels of selected candidate-biomarkers in a sample of systemic sclerosis patients with and without different forms of pulmonary hypertension. Methods: A total of 81 consecutive systemic sclerosis patients were included, 40 with systemic sclerosis pulmonary hypertension and 41 with no pulmonary hypertension. In each group, quantitative and qualitative nailfold capillaroscopy microscopy characteristics, vascular autoantibodies AT1R and ETAR, and serum levels of 24 soluble serum factors were determined. For evaluation of the nailfold capillaroscopy microscopy characteristics, linear regression analysis accounting for age, sex, and diffusing capacity of the lungs for carbon monoxide percentage predicted was used. Autoantibodies and soluble serum factor levels were compared using two-sample Results: No statistically significant differences were observed in quantitative or qualitative nailfold capillaroscopy microscopy characteristics, or vascular autoantibody ETAR and AT1R titer between systemic sclerosis-pulmonary hypertension and systemic sclerosis-no pulmonary hypertension. In contrast, several serum levels of soluble factors differed between groups: Endostatin, sVCAM, and VEGFD were increased, and CXCL4, sVEGFR2, and PDGF-AB/BB were decreased in systemic sclerosis-pulmonary hypertension. Random forest classification identified Endostatin and CXCL4 as the most predictive classifiers to distinguish systemic sclerosispulmonary hypertension from systemic sclerosis-no pulmonary hypertension. Conclusion: This study shows the potential for several soluble serum factors to distinguish systemic sclerosis-pulmonary hypertension from systemic sclerosis-no pulmonary hypertension. We found no classifying potential for qualitative or quantitative nailfold capillaroscopy microscopy characteristics, or vascular autoantibodies.
Language	English
Publishing date	2023-05-22
Publishing country	England
Document type	Journal Article
ISSN	2397-1991
ISSN (online)	2397-1991
DOI	10.1177/23971983231175213
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Article ; Online: Separating friend from foe: Inhibition of TGF-β-induced detrimental SMAD1/5/9 phosphorylation while maintaining protective SMAD2/3 signaling in OA chondrocytes.

Thielen, Nathalie G M / van Caam, Arjan P M / V Beuningen, Henk M / Vitters, Elly L / van den Bosch, Martijn H J / Koenders, Marije I / van de Loo, Fons A J / Blaney Davidson, Esmeralda N / van der Kraan, Peter M

Osteoarthritis and cartilage

2023 Volume 31, Issue 11, Page(s) 1481–1490

Abstract: Objective: Transforming growth factor-β (TGF-β) signaling via SMAD2/3 is crucial to control cartilage homeostasis. However, TGF-β can also have detrimental effects by signaling via SMAD1/5/9 and thereby contribute to diseases like osteoarthritis (OA). ... ...

Abstract	Objective: Transforming growth factor-β (TGF-β) signaling via SMAD2/3 is crucial to control cartilage homeostasis. However, TGF-β can also have detrimental effects by signaling via SMAD1/5/9 and thereby contribute to diseases like osteoarthritis (OA). In this study, we aimed to block TGF-β-induced SMAD1/5/9 signaling in primary human OA chondrocytes, while maintaining functional SMAD2/3 signaling. Design: Human OA chondrocytes were pre-incubated with different concentrations of ALK4/5/7 kinase inhibitor SB-505124 before stimulation with TGF-β. Changes in SMAD C-terminal phosphorylation were analyzed using Western blot and response genes were measured with quantitative Polymerase Chain Reaction. To further explore the consequences of our ability to separate pathways, we investigated TGF-β-induced chondrocyte hypertrophy. Results: Pre-incubation with 0.5 µM SB-505124, maintained ±50% of C-terminal SMAD2/3 phosphorylation and induction of JUNB and SERPINE1, but blocked SMAD1/5/9-C phosphorylation and expression of ID1 and ID3. Furthermore, TGF-β, in levels comparable to those in the synovial fluid of OA patients, resulted in regulation of hypertrophic and dedifferentiation markers in OA chondrocytes; i.e. an increase in COL10, RUNX2, COL1A1, and VEGF and a decrease in ACAN expression. Interestingly, in a subgroup of OA chondrocyte donors, blocking only SMAD1/5/9 caused stronger inhibition on TGF-β-induced RUNX2 than blocking both SMAD pathways. Conclusion: Our findings indicate that using low dose of SB-505124 we maintained functional SMAD2/3 signaling that blocks RUNX2 expression in a subgroup of OA patients. We are the first to show that SMAD2/3 and SMAD1/5/9 pathways can be separately modulated using low and high doses of SB-505124 and thereby split TGF-β's detrimental from protective function in chondrocytes.
MeSH term(s)	Humans ; Chondrocytes/metabolism ; Phosphorylation ; Transforming Growth Factor beta/pharmacology ; Transforming Growth Factor beta/metabolism ; Core Binding Factor Alpha 1 Subunit ; Cartilage, Articular/metabolism ; Osteoarthritis/metabolism ; Smad2 Protein/metabolism
Chemical Substances	Transforming Growth Factor beta ; Core Binding Factor Alpha 1 Subunit ; SMAD2 protein, human ; Smad2 Protein
Language	English
Publishing date	2023-08-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1167809-4
ISSN	1522-9653 ; 1063-4584
ISSN (online)	1522-9653
ISSN	1063-4584
DOI	10.1016/j.joca.2023.08.004
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Article ; Online: TGFβ/BMP Signaling Pathway in Cartilage Homeostasis.

Thielen, Nathalie G M / van der Kraan, Peter M / van Caam, Arjan P M

Cells

2019 Volume 8, Issue 9

Abstract: Cartilage homeostasis is governed by articular chondrocytes via their ability to modulate extracellular matrix production and degradation. In turn, chondrocyte activity is regulated by growth factors such as those of the transforming growth factor β ( ... ...

Abstract	Cartilage homeostasis is governed by articular chondrocytes via their ability to modulate extracellular matrix production and degradation. In turn, chondrocyte activity is regulated by growth factors such as those of the transforming growth factor β (TGFβ) family. Members of this family include the TGFβs, bone morphogenetic proteins (BMPs), and growth and differentiation factors (GDFs). Signaling by this protein family uniquely activates SMAD-dependent signaling and transcription but also activates SMAD-independent signaling via MAPKs such as ERK and TAK1. This review will address the pivotal role of the TGFβ family in cartilage biology by listing several TGFβ family members and describing their signaling and importance for cartilage maintenance. In addition, it is discussed how (pathological) processes such as aging, mechanical stress, and inflammation contribute to altered TGFβ family signaling, leading to disturbed cartilage metabolism and disease.
MeSH term(s)	Aging/metabolism ; Animals ; Bone Morphogenetic Proteins/metabolism ; Cartilage, Articular/metabolism ; Homeostasis ; Humans ; Inflammation/metabolism ; Signal Transduction ; Stress, Mechanical ; Transforming Growth Factor beta/metabolism
Chemical Substances	Bone Morphogenetic Proteins ; Transforming Growth Factor beta
Language	English
Publishing date	2019-08-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8090969
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