Interferons and systemic sclerosis: correlation between interferon gamma and interferon-lambda 1 (IL-29)

Dantas, Andréa Tavares; Gonçalves, Sayonara Maria Calado; Pereira, Michelly Cristiny; Almeida, Anderson Rodrigues de; Marques, Cláudia Diniz Lopes; Rêgo, Moacyr Jesus Barreto de Melo; Pitta, Ivan da Rocha; Duarte, Ângela Luzia Branco Pinto; Pitta, Maíra Galdino da Rocha

doi:10.3109/08916934.2015.1054028

Cited by 32 publications

(19 citation statements)

References 24 publications

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“…Expression of genes such as PLG, FGA, KLKB1, and FN1 related to hemostasis; TGFB1, IL1B was observed in this CD4 + CTL subset, corroborating similar findings from the above tissue studies ( Figure 7B). Expanding upon our observations that CD4 + CTLs accumulate in both the vascular and tissue compartments of SSc patients, we curated a collection of gene sets relevant to tissue remodeling by type I and type II interferons, both of which have been implicated in the pathogenesis of systemic sclerosis (43)(44)(45). Overall, these findings are consistent with the notion that CD28 lo CD57 hi CD4 + CTLs represent an activated effector population of CD4 + T cells involved in the ongoing immune response at the time of sample collection rather than a resting memory or exhausted T cell population.…”

Section: Resultsmentioning

confidence: 99%

Cytotoxic CD4+ T lymphocytes may induce endothelial cell apoptosis in systemic sclerosis

Mitsui

Kaneko

Perugino

et al. 2020

Journal of Clinical Investigation

122

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Section: Resultsmentioning

confidence: 99%

Cytotoxic CD4+ T lymphocytes may induce endothelial cell apoptosis in systemic sclerosis

Mitsui

Kaneko

Perugino

et al. 2020

Journal of Clinical Investigation

122

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“…Lung fibrosis was observed using high-resolution computed tomography (HRCT); esophagus involvement was determined by scintillography and/or endoscopy; proximal muscle weakness and elevated serum creatine kinase indicated muscle involvement. Pulmonary artery pressure was estimated by Doppler echocardiogram; pressures above 35 mmHg were interpreted as pulmonary hypertension [15, 16]. The modified Rodnan total skin thickness score (mRSS) was used to evaluate skin fibrosis [17].…”

Section: Methodsmentioning

confidence: 99%

Reassessing the Role of the Active TGF-β1 as a Biomarker in Systemic Sclerosis: Association of Serum Levels with Clinical Manifestations

Dantas

Gonçalves²,

Almeida³

et al. 2016

Disease Markers

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Objective. To determine active TGF-β1 (aTGF-β1) levels in serum, skin, and peripheral blood mononuclear cell (PBMC) culture supernatants and to understand their associations with clinical parameters in systemic sclerosis (SSc) patients. Methods. We evaluated serum samples from 56 SSc patients and 24 healthy controls (HC). In 20 SSc patients, we quantified spontaneous or anti-CD3/CD28 stimulated production of aTGF-β1 by PBMC. The aTGF-β1 levels were measured by ELISA. Skin biopsies were obtained from 13 SSc patients and six HC, and TGFB1 expression was analyzed by RT-PCR. Results. TGF-β1 serum levels were significantly higher in SSc patients than in HC (p < 0.0001). Patients with increased TGF-β1 serum levels were more likely to have diffuse subset (p = 0.02), digital ulcers (p = 0.02), lung fibrosis (p < 0.0001), positive antitopoisomerase I (p = 0.03), and higher modified Rodnan score (p = 0.046). Most of our culture supernatant samples had undetectable levels of TGF-β1. No significant difference in TGFB1 expression was observed in the SSc skin compared with HC skin. Conclusion. Raised active TGF-β1 serum levels and their association with clinical manifestations in scleroderma patients suggest that this cytokine could be a marker of fibrotic and vascular involvement in SSc.

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“…Serum levels of IL‐29 were higher in HT patients as compared to healthy controls . Furthermore, systemic sclerosis (SSc) patients showed increased IL‐29 serum levels as compared to that in healthy controls . Childhood uveitis is a sight‐threatening inflammatory eye disease.…”

Section: Il‐29 and Inflammatory Autoimmune Diseasesmentioning

confidence: 99%

Insights into IL‐29: Emerging role in inflammatory autoimmune diseases

Wang

Huang

et al. 2019

J Cellular Molecular Medi

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Interleukin‐29 (IL‐29) is a newly discovered member of type III interferon. It mediates signal transduction via binding to its receptor complex and activates downstream signalling pathways, and therefore induces the generation of inflammatory components. Recent studies reported that expression of IL‐29 is dysregulated in inflammatory autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, Sjögren's syndrome, psoriasis and systemic sclerosis. Furthermore, functional analysis revealed that IL‐29 may involve in the pathogenesis of the inflammatory autoimmune disorders. In this review, we will systematically review the current knowledge about IL‐29. The information collected revealed the regulatory role of IL‐29 and may give important implications for its potential in clinical treatment.

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Interferons and systemic sclerosis: correlation between interferon gamma and interferon-lambda 1 (IL-29)

Abstract: We first showed raised IFN-λ1 levels in SSc patients. Furthermore, we found a correlation between IFN-λ1 and IFN-γ levels and an association between IFN-γ and myositis. Additional in vitro and in vivo studies are needed to understand IFN-λ1 role in SSc.

Cited by 32 publications

References 24 publications

Cytotoxic CD4+ T lymphocytes may induce endothelial cell apoptosis in systemic sclerosis

Cytotoxic CD4+ T lymphocytes may induce endothelial cell apoptosis in systemic sclerosis

Reassessing the Role of the Active TGF-β1 as a Biomarker in Systemic Sclerosis: Association of Serum Levels with Clinical Manifestations

Insights into IL‐29: Emerging role in inflammatory autoimmune diseases

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