Human activated CD4+ T lymphocytes increase IL-2 expression by downregulating microRNA-181c

Xue, Qingwu; Z, Guo; Li, Wei; Wen, Weihong; Meng, Yanyan; Jia, Lintao; Wang, Jian; Yao, Libo; Jin, Boquan; Wang, Tao; Yang, Angang

doi:10.1016/j.molimm.2010.10.021

Cited by 74 publications

(65 citation statements)

References 28 publications

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“…For example, miR-181c was downregulated in the process of CD4? T lymphocyte cell activation [9]. Furthermore, miR-181c acts as a suppressor of human PBMC CD4?…”

Section: Introductionmentioning

confidence: 99%

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

et al. 2015

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miR-181c is a newly identified negative regulator of immune cell activation. In this study, we aimed to investigate the expression and functional role of miR-181c in myasthenia gravis (MG). miR-181c showed significant downregulation in peripheral blood mononuclear cells (PBMCs) from MG patients compared with healthy controls, with lower expression in generalized patients than in ocular ones. MG patients also had increased serum IL-7 and IL-17 levels. Additionally, serum IL-7 level presents a positive correlation with the serum IL-17 level. miR-181c levels were negatively correlated with serum levels of IL-7 and IL-17 in either generalized patients or ocular patients. A luciferase reporter assay revealed that miR-181c could directly bind to the 3'-UTR of interleukin-7. Forced expression of miR-181c led to decreased IL-7 and IL-17 release in cultured PBMCs, while depletion of miR-181c increased the secretion of these two proinflammatory cytokines. The results from our study suggested for the first time that miR-181c was able to negatively regulate the production of proinflammatory cytokines IL-7 and IL-17 in MG patients, and it is a novel potential therapeutic target for MG.

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“…For example, miR-181c was downregulated in the process of CD4? T lymphocyte cell activation [9]. Furthermore, miR-181c acts as a suppressor of human PBMC CD4?…”

Section: Introductionmentioning

confidence: 99%

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

et al. 2015

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“…For example, miR-181c inhibits IL-2 expression by directly binding to its 3 UTR. This repression is reversed upon T-cell activation that downregulates miR-181c expression [38]. By contrast, miR-31 was found to be upregulated upon TCR stimulation and to increase IL-2 production [39].…”

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confidence: 99%

Cross‐regulation between cytokine and microRNA pathways in T cells

et al. 2015

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microRNA (miRNA) mediated regulation of protein expression has emerged as an important mechanism in T-cell physiology, from development and survival to activation, proliferation, and differentiation. One of the major classes of proteins involved in these processes are cytokines, which are both key input signals and major products of T-cell function. Here, we summarize the current data on the molecular cross-talk between cytokines and miRNAs: how cytokines regulate miRNA expression, and how specific miRNAs control cytokine production in T cells. We also describe the inflammatory consequences of deregulating the miRNA/cytokine axis in mice and humans. We believe this topical area will have key implications for immune modulation and treatment of autoimmune pathology. Keywords:Cytokines r Inflammation r miRNA r T cells microRNAs as regulators of protein expressionBiological processes require the integration of environmental stimuli at the level of gene expression. The robustness of genetic networks depends on the distinction between physiological responses (to particular cues) and biological "noise" (stochastic variations), which can be achieved, for example, by establishing feed-forward transcriptional loops. Over the past two decades, a new mechanism that interacts with transcriptional loops and sets additional thresholds, which enable cells to filter physiological signals from noise has emerged; this mechanism regulates gene expression at the posttranscriptional level and relies on microRNAs (miRNAs; reviewed in [1]). These are an abundant class of evolutionarily conserved small noncoding (untranslated) RNA species that control target mRNA stability, degradation, and translation, thus affecting the majority of mammalian genes [2].Correspondence: Dr. Anita Q. Gomes e-mail: anitagomes@medicina.ulisboa.ptIn the conventional miRNA biogenesis pathway, RNA polymerase II transcribed pri-miRNAs are processed by the nuclear RNase III enzyme Drosha (complexed with DGCR8) to generate 60-70 nt stem-loop intermediates, the pre-miRNAs, that are further processed into 19-24mers in the cytoplasm by another key RNase III, Dicer. Mature miRNAs are then incorporated into RNAinduced silencing complexes, whose core components are proteins of the Argonaute family (Ago1-4), which use the 5 end (nucleotides 2-8) "seed sequence" of the miRNA to recognize complementary mRNA transcripts (mostly in their 3 untranslated region) for deadenylation or inhibition of translation, ultimately resulting in mRNA decapping and decay (reviewed in [3,4]).Unique spatial and temporal expression patterns in distinct hematopoietic cell lineages are suggestive of multiple roles for miRNAs in hematopoiesis, self-tolerance, and in immune responses, which have been explored over the past decade (reviewed in [5,6]). Over a 100 different miRNAs have been shown to be expressed by cells of the immune system, where * These authors contributed equally to this work as first authors. * * These authors contributed equally to this work as last authors.C 2015 WILEY-VCH Ve...

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“…guidelines on the detection and monitoring of endocrine abnormalities post-TBI in the clinic may provide a guideline for treatment of depression and diminish the severity of depression symptoms and ultimately improve quality of life [51]. Cortisol administration showed efficacy as a treatment for depressed patients with hypocortisolemia following TBI.…”

Section: Discussionmentioning

confidence: 99%

Cortisol Supplement Combined with Psychotherapy and Citalopram Improves Depression Outcomes in Patients with Hypocortisolism after Traumatic Brain Injury

Luo¹,

Chai²,

Jiang³

et al. 2015

Aging and disease

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Depression is one of the most prevalent psychiatric disorders in people with Traumatic brain injury (TBI). Depression after TBI is closely related with social and psychological factors and hypothalamicpituitary -adrenal (HPA) axis dysfunction. However, there is a lack of evidence regarding effective treatment approaches for depression. A total of 68 patients with depression following closed TBI were recruited. Glasgow Coma Scale score (GCS) was employed to demonstrate the severity of neurological deficits and Glasgow Outcome Scale (GOS) was employed to measure functional outcome after TBI. The severity of depression was quantified using the Beck Depression Inventory-II (BDI-II) in line with DSM-IV. Citalopram and Prednisone were administered to subjects with normal cortisol levels or hypocortisolism separately, based on psychotherapeutic interventions. We investigated the relationship between degree of depression of TBI patients and the severity and progression of TBI with the therapeutic effects of Citalopram in combination with psychotherapeutic and Prednisone in depressed patients. There was no relationship between the severity of depression and the severity and progression of TBI. The basic treatment of psychotherapeutic interventions could partially relieve depressive symptoms. Combination of psychotherapeutic support and Citalopram significantly improved depressive symptoms in patients with normal cortisol levels, but not in hypocortisolic patients. Combination of Prednisone administration with psychotherapeutic treatment and Citalopram significantly improved depression outcome in hypocortisolic patients after TBI. Hypocortisolism after TBI may regulate depression. Combination of Prednisone with psychotherapeutic treatment and Citalopram may provide better therapeutic effects in depression patients with hypocortisolism after TBI.

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Human activated CD4+ T lymphocytes increase IL-2 expression by downregulating microRNA-181c

Cited by 74 publications

References 28 publications

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

Cross‐regulation between cytokine and microRNA pathways in T cells

Cortisol Supplement Combined with Psychotherapy and Citalopram Improves Depression Outcomes in Patients with Hypocortisolism after Traumatic Brain Injury

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