Role of syndecan-1 in the interaction between dendritic cells and T cells

Kouwenberg, M.; Rops, Angelique L.; Bebber, Marinka Bakker-van; Diepeveen, Laura E.; Götte, Martin; Hilbrands, Luuk B.; Vlag, Johan van der

doi:10.1101/2020.03.11.987602

Cited by 2 publications

(2 citation statements)

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“…In addition to the activation of macrophages, T cells, and FLS, IL-34 may promote synovial inflammation by the initiation of osteoclastogenesis (43). Of note, osteoclastogenesis and osteoporosis are prominent in synovial inflammation (49)(50)(51)(52). Indeed, the imbalance between M1 and M2 macrophages in RA patients has been linked to increased occurrence of osteoclastogenesis in RA patients (16).…”

Section: Il-in Ramentioning

confidence: 99%

“…In addition to CSF-1R, syndecan-1 (CD138) and protein tyrosine phosphatase receptor type ζ1 (PTPRZ1) bind IL-34 (Figure 1). Syndecan-1 is a cell surface proteoglycan functioning as a co-receptor to various cell surface receptors (56) and, besides, a regulatory factor involved in cell adhesion and cell migration (49)(50)(51)(52). Syndecan-1 is present in various human subsets of monocytes and macrophages (57).…”

Section: Il-in Ramentioning

confidence: 99%

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Interleukin-34-regulated T-cell responses in rheumatoid arthritis

Park

Baek

2022

Front. Med.

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Rheumatoid arthritis (RA) is a chronic autoimmune disease with a multifaceted etiology, which primarily affects and results in the deterioration of the synovium of patients. While the exact etiology of RA is still largely unknown, there is growing interest in the cytokine interleukin-34 (IL-34) as a driver or modulator of RA pathogenesis on the grounds that IL-34 is drastically increased in the serum and synovium of RA patients. Several studies have so far revealed the relationship between IL-34 levels and RA disease progression. Nevertheless, the significance and role of IL-34 in RA have remained ambiguous, as illustrated by two most recent studies, which reported contrasting effects of genetic IL-34 deletion in RA. Of note, IL-34 is a macrophage growth factor and is increasingly perceived as a master regulator of T-cell responses in RA via macrophage-dependent as well as T cell-intrinsic mechanisms. In this regard, several studies have demonstrated that IL-34 potentiates helper T-cell (Th) responses in RA, whereas studies also suggested that IL-34 alleviates synovial inflammation, potentially by inducing regulatory T-cells (Treg). Herein, we provide an overview of the current understanding of IL-34 involvement in RA and outline IL-34-mediated mechanisms in regulating T-cell responses in RA.

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Section: Il-in Ramentioning

confidence: 99%

Section: Il-in Ramentioning

confidence: 99%

Interleukin-34-regulated T-cell responses in rheumatoid arthritis

Park

Baek

2022

Front. Med.

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Altered Serum Proteins Suggest Inflammation, Fibrogenesis and Angiogenesis in Adult Patients with a Fontan Circulation

Michel,

Renaud,

Schmidt

et al. 2024

IJMS

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Previous omics research in patients with complex congenital heart disease and single-ventricle circulation (irrespective of the stage of palliative repair) revealed alterations in cardiac and systemic metabolism, inter alia abnormalities in energy metabolism, and inflammation, oxidative stress or endothelial dysfunction. We employed an affinity-proteomics approach focused on cell surface markers, cytokines, and chemokines in the serum of 20 adult Fontan patients with a good functioning systemic left ventricle, and we 20 matched controls to reveal any specific processes on a cellular level. Analysis of 349 proteins revealed 4 altered protein levels related to chronic inflammation, with elevated levels of syndecan-1 and glycophorin-A, as well as decreased levels of leukemia inhibitory factor and nerve growth factor-ß in Fontan patients compared to controls. All in all, this means that Fontan circulation carries specific physiological and metabolic instabilities, including chronic inflammation, oxidative stress imbalance, and consequently, possible damage to cell structure and alterations in translational pathways. A combination of proteomics-based biomarkers and the traditional biomarkers (uric acid, γGT, and cholesterol) performed best in classification (patient vs. control). A metabolism- and signaling-based approach may be helpful for a better understanding of Fontan (patho-)physiology. Syndecan-1, glycophorin-A, leukemia inhibitory factor, and nerve growth factor-ß, especially in combination with uric acid, γGT, and cholesterol, might be interesting candidate parameters to complement traditional diagnostic imaging tools and the determination of traditional biomarkers, yielding a better understanding of the development of comorbidities in Fontan patients, and they may play a future role in the identification of targets to mitigate inflammation and comorbidities in Fontan patients.

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Role of syndecan-1 in the interaction between dendritic cells and T cells

Cited by 2 publications

References 48 publications

Interleukin-34-regulated T-cell responses in rheumatoid arthritis

Interleukin-34-regulated T-cell responses in rheumatoid arthritis

Altered Serum Proteins Suggest Inflammation, Fibrogenesis and Angiogenesis in Adult Patients with a Fontan Circulation

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