Microarray analysis of microRNA expression in peripheral blood cells of systemic lupus erythematosus patients

Dai, Yong; Huang, Yi; Tang, Min; Lv, Tianjing; Hu, Chaofan; Yue-jin, Tan; Xu, Zhongneng; Yin, Yibing

doi:10.1177/0961203307084158

Cited by 332 publications

(245 citation statements)

References 37 publications

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“…The strong association between the miR-146a level and clinical disease activity indicates that it may serve as a new disease biomarker. Dai et al (42) recently identified several differentially expressed miRNA in lupus patients by microarray analysis; however, dysregulation of miR-146a was not reported. This is likely due to the difference between the quantification methods and patient cohorts used in their study as compared with ours.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐146a contributes to abnormal activation of the type I interferon pathway in human lupus by targeting the key signaling proteins

Tang

Luo

Cui

et al. 2009

Arthritis & Rheumatism

673

574

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ObjectiveMicroRNA have recently been identified as regulators that modulate target gene expression and are involved in shaping the immune response. This study was undertaken to investigate the contribution of microRNA‐146a (miR‐146a), which was identified in the pilot expression profiling step, to the pathogenesis of systemic lupus erythematosus (SLE).MethodsTaqMan microRNA assays of peripheral blood leukocytes were used for comparison of expression levels of microRNA between SLE patients and controls. Transfection and stimulation of cultured cells were conducted to determine the biologic function of miR‐146a. Bioinformatics prediction and validation by reporter gene assay and Western blotting were performed to identify miR‐146a targets.ResultsProfiling of 156 miRNA in SLE patients revealed the differential expression of multiple microRNA, including miR‐146a, a negative regulator of innate immunity. Further analysis showed that underexpression of miR‐146a negatively correlated with clinical disease activity and with interferon (IFN) scores in patients with SLE. Of note, overexpression of miR‐146a reduced, while inhibition of endogenous miR‐146a increased, the induction of type I IFNs in peripheral blood mononuclear cells (PBMCs). Furthermore, miR‐146a directly repressed the transactivation downstream of type I IFN. At the molecular level, miR‐146a could target IFN regulatory factor 5 and STAT‐1. More importantly, introduction of miR‐146a into the patients' PBMCs alleviated the coordinate activation of the type I IFN pathway.ConclusionThe microRNA miR‐146a is a negative regulator of the IFN pathway. Underexpression of miR‐146a contributes to alterations in the type I IFN pathway in lupus patients by targeting the key signaling proteins. The findings provide potential novel strategies for therapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐146a contributes to abnormal activation of the type I interferon pathway in human lupus by targeting the key signaling proteins

Tang

Luo

Cui

et al. 2009

Arthritis & Rheumatism

673

574

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“…By targeting the key signaling components, decreased levels of miR-146a lead to increased type I IFN pathway activity in lupus patients [16]. In addition, Dai et al [17] identified 16 miRNAs that are differentially expressed in SLE.…”

Section: Systemic Lupus Erythematosusmentioning

confidence: 99%

Epigenetics in autoimmune disorders: Highlights of the 10th Sjögren's Syndrome Symposium

Lu¹,

Renaudineau²,

Cha

et al. 2010

Autoimmunity Reviews

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During the 10th International Symposium on Sjögren's Syndrome held in Brest, France, from October 1-3, 2009 (http://www.sjogrensymposium-brest2009.org), the creation of an international epigenetic autoimmune group has been proposed to establish gold standards and to launch collaborative studies. During this "epigenetics session", leading experts in the field presented and discussed the most recent developments of this topic in Sjögren's Syndrome research. The "Brest epigenetic task force" was born and has scheduled a meeting in Ljubljana, Slovenia during the 7th Autoimmunity congress in May 2010.The following is a report of that session.  Increased activity and destructive potential of synovial fibroblasts in rheumatoid arthritis is due in part to the deregulation of epigenetic factors. Development of an epigenetic bank and the establishment of gold standards in an epigenetic consortium to analyse epigenetic modifications are needed. Epigenetic alterations in autoimmune diseases could be used as prognostic/diagnostic tools and markers of immune cell activation.2

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“…Recently, aberrant expression of miRNAs was observed in patients with SLE [34][35][36][37] and murine models of lupus [38]. Therefore, miRNAs could regulate CD1d expression.…”

Section: Introductionmentioning

confidence: 99%

TLR9‐induced miR‐155 and Ets‐1 decrease expression of CD1d on B cells in SLE

et al. 2015

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B cells present lipid antigens to CD1d-restricted invariant natural killer T (iNKT) cells to maintain autoimmune tolerance, and this process is disrupted in systemic lupus erythematosus (SLE). Inflammation may inhibit CD1d expression to exacerbate the pathology of lupus. However, how inflammation regulates CD1d expression on B cells is unclear in SLE.In the present study, we showed that the surface expression of CD1d on B cells from SLE mice was decreased and that stimulation of inflammatory responses through TLR9 decreased the membrane and total CD1d levels of CD1d on B cells. Moreover, inflammation-related microRNA-155 (miR-155) negatively correlated with the expression of CD1d in B cells. miR-155 directly targeted the 3 -untranslated region (3 -UTR) of CD1d upon TLR9 activation in both humans and mice. The inhibitory effects of miR-155 on CD1d expression in B cells impaired their antigen-presenting capacity to iNKT cells. In addition, Ets-1, a susceptibility gene of SLE, also directly regulated the expression of the CD1d gene at the transcriptional level. These findings provide new insight into the mechanism underlying decreased CD1d expression on B cells in SLE, suggesting that inhibition of inflammation may increase CD1d expression in B cells to ameliorate SLE via modulating iNKT cells.Keywords: B cells r CD1d r Ets-1 r miR-155 r SLE Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionSystemic lupus erythematosus (SLE) is a complex and chronic autoimmune disease with an unclear etiology [1]. B cells play a central role in the pathogenesis of SLE [2], and patients with SLE exhibit abnormal B-cell activation and increased sensitivity and proliferation of B cells [3]. Moreover, the Correspondence: Dr. Yayi Hou e-mail: yayihou@nju.edu.cn clinical success of B-cell depletion therapy further proves the important role of B cells in SLE pathogenesis [4,5]. B cells not only produce antibodies and release cytokines and chemokines but also present both peptide and lipid antigens [6].CD1 family molecules are nonclassical MHC proteins related to the class I MHC proteins and are involved in the presentation of lipid antigens to T cells. Several studies have suggested that CD1d may play an immunoregulatory role in the development of lupus, and CD1d deficiency exacerbates lupus nephritis in the pristineinduced model [7] and inflammatory dermatitis in MRL-lpr/lpr C 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2015. 45: 1934-1945 Cellular immune response 1935 mice [8]. Importantly, endogenous DNA stimulates inflammatory responses through TLR9 and exacerbates lupus disease pathology [9,10]. Viral infection could downregulate the expression of CD1d in APCs, such as B cells [11,12], DCs, and macrophages [13]. A number of exogenous viruses, especially Epstein-Barr virus (EBV) [14,15], also have been linked to the pathogenesis of SLE [16]. Our previous studies have indicated that ligands for both TLR9 and TLR7 lead to B...

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Microarray analysis of microRNA expression in peripheral blood cells of systemic lupus erythematosus patients

Cited by 332 publications

References 37 publications

MicroRNA‐146a contributes to abnormal activation of the type I interferon pathway in human lupus by targeting the key signaling proteins

MicroRNA‐146a contributes to abnormal activation of the type I interferon pathway in human lupus by targeting the key signaling proteins

Epigenetics in autoimmune disorders: Highlights of the 10th Sjögren's Syndrome Symposium

TLR9‐induced miR‐155 and Ets‐1 decrease expression of CD1d on B cells in SLE

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