Chemokines in systemic sclerosis

King, Ji Jade; Abraham, David; Stratton, Richard

doi:10.1016/j.imlet.2017.12.001

Cited by 16 publications

(24 citation statements)

References 81 publications

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“…In inflammatory conditions, this cytokine network may induce fibroblast activation, leading to the production of various chemokines, such as monocyte chemoattractant protein-1 and IFN-γ-induced protein-10 [ 49 ]. Aberrant chemokine production by fibroblasts attracts lymphocytes, and as infiltrated lymphocytes in turn release pro-inflammatory cytokines, an inflammatory loop may ensue [ 50 ]. Thus, JAK inhibitors are expected to show at least comparable efficacy to IL-6 signalling blockade, and may potentially exert greater efficacy than tocilizumab by inhibiting a broad array of cytokine signalling.…”

Section: Discussionmentioning

confidence: 99%

In vitro pharmacological effects of peficitinib on lymphocyte activation: a potential treatment for systemic sclerosis with JAK inhibitors

et al. 2019

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Objectives Peficitinib, a novel Janus kinase (JAK) inhibitor, demonstrated promising results in treating RA in phase 3 clinical trials. This in vitro study was undertaken to characterize the pharmacological properties of peficitinib and investigate the involvement of JAK and signal transducer and activator of transcription (STAT) pathways in the pathological processes of SSc, which is also an autoimmune disease. Methods Phosphorylation levels of STAT molecules were assessed in peripheral blood mononuclear cells collected from patients with RA or SSc and healthy subjects, and in skin specimens obtained from 19 patients with SSc. In vitro inhibition of STAT phosphorylation and cytokine/chemokine production by peficitinib, tofacitinib and baricitinib were also characterized. Results Higher spontaneous STAT1 or STAT3 phosphorylation was observed in peripheral T-cells and monocytes from patients with RA and SSc compared with healthy subjects. In skin sections from patients with SSc, phosphorylated STAT3–positive cells were found in almost all cases, irrespective of disease subtype or patient characteristics. Conversely, phosphorylated STAT1-positive cells were observed only in samples from untreated patients with diffuse disease of short duration. Peficitinib inhibited STAT phosphorylation induced by various cytokines, with comparable efficacy to tofacitinib and baricitinib. Peficitinib also suppressed cytokine and chemokine production by peripheral blood mononuclear cells and skin fibroblasts. Conclusion Our results suggest that JAK/STAT pathways are constitutively activated in SSc and RA, and that the JAK inhibitor may represent a novel therapeutic option for SSc.

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Section: Discussionmentioning

confidence: 99%

In vitro pharmacological effects of peficitinib on lymphocyte activation: a potential treatment for systemic sclerosis with JAK inhibitors

et al. 2019

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“…Chemokines are substances originally found as mediators of cell recruitment. Accumulating evidence has demonstrated that chemokines affect many biological processes other than chemotaxis, such as cell growth, embryonic development, autoimmunity, inflammation, and angiogenesis 4,5 . Altered expression profiles of chemokines have been shown in various pathological conditions, including autoimmune diseases, and SSc is no exception.…”

Section: Introductionmentioning

confidence: 99%

“…Altered expression profiles of chemokines have been shown in various pathological conditions, including autoimmune diseases, and SSc is no exception. For example, CCL3 and CCL5 contribute to the early stage of SSc by recruiting mononuclear cells and causing related tissue damage 4 . In the later stages of SSc, CCL2, CCL7, CXCL10, and CXCL12 work together in promoting sclerotic changes across multiple organs 4 .…”

Section: Introductionmentioning

confidence: 99%

“…For example, CCL3 and CCL5 contribute to the early stage of SSc by recruiting mononuclear cells and causing related tissue damage 4 . In the later stages of SSc, CCL2, CCL7, CXCL10, and CXCL12 work together in promoting sclerotic changes across multiple organs 4 . In addition, serum levels of CCL18 and CXCL4 serve as useful markers for the activity of interstitial lung disease associated with SSc 6,7 .…”

Section: Introductionmentioning

confidence: 99%

“…Accumulating evidence has demonstrated that chemokines affect many biological processes other than chemotaxis, such as cell growth, embryonic development, autoimmunity, inflammation, and angiogenesis. 4,5 Altered expression profiles of chemokines have been shown in various pathological conditions, including autoimmune diseases, and SSc is no exception. For example, CCL3 and CCL5 contribute to the early stage of SSc by recruiting mononuclear cells and causing related tissue damage.…”

Section: Introductionmentioning

confidence: 99%

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Association of serum CXCL12 levels with arthropathy in patients with systemic sclerosis

et al. 2020

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Aim Systemic sclerosis (SSc) is an autoimmune connective tissue disease, in which extensive fibrotic change and vasculopathy affect the skin and various internal organs. It also involves the joints, causing stiffness, arthralgia, and arthritis. Although arthropathy is commonly observed in SSc, its underlying mechanism remains unknown. CXCL12, also known as stromal cell derived factor 1, is associated with inflammation, mesenchymal cell recruitment, angiogenesis, and collagen production, and is implicated in the development of various joint diseases. To assess the potential contribution of CXCL12 to SSc development, we investigated the clinical association of serum CXCL12 levels in patients with SSc. Method We conducted a cross‐sectional analysis of 68 patients with SSc and 20 healthy controls recruited in a single center over 9 years. Serum CXCL12 levels were measured by enzyme‐linked immunosorbent assay. Results Serum CXCL12 levels were significantly higher in patients with SSc than in healthy controls (median 1554.0 pg/mL, 25th‐75th centiles 1313.0‐1914.0 pg/mL vs 967.4 pg/mL, 608.8‐1271.0 pg/mL, P < 0.001). Patients with SSc with elevated CXCL12 levels had significantly more cases of arthropathy than those with normal CXCL12 levels (85.7% vs 25.0%, P = 0.01). Furthermore, patients with SSc with elevated CXCL12 levels showed an increased trend in the prevalence of limited range of motion of the finger joints compared with those with normal CXCL12 levels (60.0% vs 18.6%, P =0 .07). Moreover, serum CXCL12 levels were significantly correlated with the titers of rheumatoid factor in patients with SSc (r = .41, P = 0.001). Conclusion Elevated serum CXCL12 levels may be related to the development of SSc arthropathy.

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Using the Bleomycin-Induced Model of Fibrosis to Study the Contribution of CCN Proteins to Scleroderma Fibrosis

Peidl

Nguyen

Chitturi

et al. 2022

Methods in Molecular Biology

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Chemokines in systemic sclerosis

Cited by 16 publications

References 81 publications

In vitro pharmacological effects of peficitinib on lymphocyte activation: a potential treatment for systemic sclerosis with JAK inhibitors

In vitro pharmacological effects of peficitinib on lymphocyte activation: a potential treatment for systemic sclerosis with JAK inhibitors

Association of serum CXCL12 levels with arthropathy in patients with systemic sclerosis

Using the Bleomycin-Induced Model of Fibrosis to Study the Contribution of CCN Proteins to Scleroderma Fibrosis

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