Simultaneously increased expression of micro<scp>RNA</scp>‐155 and suppressor of cytokine signaling 1 (<i><scp>SOCS</scp>1</i>) gene in the peripheral blood mononuclear cells of patients with primary Sjögren's syndrome

Chen, Ji-Qing; Zilahi, Erika; Papp, Gábor; Sipka, Sándor; Zeher, Margit

doi:10.1111/1756-185x.12804

Cited by 19 publications

(12 citation statements)

References 24 publications

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“…General limitations of these studies are small sample sizes, heterogeneous clinical parameters and potential confounding of the results by variation in cell type distribution. A consistent finding of several studies is upregulated expression of miR-146a/b in PBMCs from patients with pSS [ 81 , 83 , 84 , 86 ]. A proposed mechanism for miR-146-dependent regulation of immune responses is via negative feedback mechanisms targeting TLR signalling [ 106 , 107 ]; dysregulated miR-146 expression may promote excess inflammation, leading to autoimmune responses.…”

Section: Ncrnassupporting

confidence: 84%

Genetics and epigenetics in primary Sjögren’s syndrome

et al. 2021

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Primary Sjögren’s syndrome (pSS) is considered to be a multifactorial disease, where underlying genetic predisposition, epigenetic mechanisms and environmental factors contribute to disease development. In the last 5 years, the first genome-wide association studies in pSS have been completed. The strongest signal of association lies within the HLA genes, whereas the non-HLA genes IRF5 and STAT4 show consistent associations in multiple ethnicities but with a smaller effect size. The majority of the genetic risk variants are found at intergenic regions and their functional impact has in most cases not been elucidated. Epigenetic mechanisms such as DNA methylation, histone modifications and non-coding RNAs play a role in the pathogenesis of pSS by their modulating effects on gene expression and may constitute a dynamic link between the genome and phenotypic manifestations. This article reviews the hitherto published genetic studies and our current understanding of epigenetic mechanisms in pSS.

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Section: Ncrnassupporting

confidence: 84%

Genetics and epigenetics in primary Sjögren’s syndrome

et al. 2021

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“…Our data would imply that this is probably not the case, since the expression of both SOCS1 and SOCS3 mRNA was found to be increased in pSS patients compared with healthy controls. Increased local or systemic expression of SOCS1 and SOCS3 in patients with pSS was also demonstrated in two recent studies [31,32]. We hypothesize that up-regulated SOCS1 expression in circulating PBMCs from pSS patients may prevent constitutive STAT1 phosphorylation in these cells that are normally exposed to rather low levels of STAT1-activating cytokines.…”

Section: Discussionsupporting

confidence: 63%

Cytokine-induced STAT1 activation is increased in patients with primary Sjögren's syndrome

Pertovaara

Silvennoinen

Isomäki

2016

Clinical Immunology

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“…Increased expression of miR-155 has been demonstrated in the context of several autoimmune diseases, such as in whole peripheral blood in lupus patients (39) and in blood mononuclear cells in patients with primary Sjögren syndrome (40). In RA, miR-155 has been found elevated in PBMCs (41) and blood monocytes (42,43) but also in synovial tissue both in synovial B cells (44) and in synovial monocytes and macrophages (22).…”

Section: Discussionmentioning

confidence: 99%

Monocyte/Macrophage Abnormalities Specific to Rheumatoid Arthritis Are Linked to miR-155 and Are Differentially Modulated by Different TNF Inhibitors

Paoletti

Rohmer

et al. 2019

The Journal of Immunology

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Proinflammatory macrophages and miR-155 are increased in patients with rheumatoid arthritis (RA). We studied membrane TNF (mTNF) expression on blood monocytes, polarization into macrophages, miR-155 expression, and the effect of anti-TNF on these biomarkers in RA patients. Sixty-seven RA patients and 109 controls (55 healthy, 54 with spondyloarthritis and connective tissue diseases) were studied. Monocytes were isolated and differentiated into macrophages with or without anti-TNF. mTNF expression was increased on monocytes from RA patients, but not from other inflammatory diseases, correlated with disease activity. Under human serum AB or M-CSF, only monocytes from RA had a defect of differentiation into M2-like macrophages and had a propensity for preferential maturation toward M1-like macrophages that contributed to synovial inflammation. This defect was correlated to mTNF expression and was partially reversed by monoclonal anti-TNF Abs but not by the TNF soluble receptor. miR-155 was increased in M2-macrophages except in adalimumab-treated patients. Transfection of healthy monocytes with miR-155 induced a decrease in M2-like markers, and transfection of RA monocytes with antagomir-155 allowed restoration of M2-like polarization. Defect in differentiation of monocytes into M2-like-macrophages linked to increased miR-155 and correlated with increased mTNF on monocytes could play a key role in RA pathogenesis. Monoclonal anti-TNF Abs but not the TNF soluble receptor partially restored this defect.

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Simultaneously increased expression of microRNA‐155 and suppressor of cytokine signaling 1 (SOCS1) gene in the peripheral blood mononuclear cells of patients with primary Sjögren's syndrome

Abstract: This unanticipated phenomenon might be a laboratory characteristic of Sjögren's syndrome, and presumably a consequence of the noteworthy difference in the pSS immune system reacting with Epstein-Barr virus.

Cited by 19 publications

References 24 publications

Genetics and epigenetics in primary Sjögren’s syndrome

Genetics and epigenetics in primary Sjögren’s syndrome

Cytokine-induced STAT1 activation is increased in patients with primary Sjögren's syndrome

Monocyte/Macrophage Abnormalities Specific to Rheumatoid Arthritis Are Linked to miR-155 and Are Differentially Modulated by Different TNF Inhibitors

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