miR-155 indicates the fate of CD4+ T cells

Chen, Li; Gao, Dian; Shao, Zhaozhao; Zheng, Qiaoyu; Yu, Qianli

doi:10.1016/j.imlet.2020.05.003

Cited by 23 publications

(15 citation statements)

References 164 publications

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“…MiR-30b, miR-125a, miR-99a, miR-17 and miR-23b were previously demonstrate to be dysregulated in tolerogenic dendritic cells (DC) 13 . MiR-155 exerts a central role in the maturation of B-cells and plasma cell commitment 14 – 17 and in the differentiation of T helper cells 18 . MiR-17–92 cluster was shown to regulate B-cell proliferation, development and immunoglobulin rearrangement by targeting Bim and PTEN 19 .…”

Section: Resultsmentioning

confidence: 99%

Differential expression of circulating miRNAs after alemtuzumab induction therapy in lung transplantation

Benazzo

Beigrezaei

Auner

et al. 2022

Sci Rep

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Alemtuzumab is a monoclonal antibody targeting CD52, used as induction therapy after lung transplantation (LTx). Its engagement produces a long-lasting immunodepletion; however, the mechanisms driving cell reconstitution are poorly defined. We hypothesized that miRNAs are involved in this process. The expression of a set of miRNAs, cytokines and co-signaling molecules was measured with RT-qPCR and flow cytometry in prospectively collected serum samples of LTx recipients, after alemtuzumab or no induction therapy. Twenty-six LTx recipients who received alemtuzumab and twenty-seven matched LTx recipients without induction therapy were included in the analysis. One year after transplantation four miRNAs were differentially regulated: miR-23b (p = 0.05) miR-146 (p = 0.04), miR-155 (p < 0.001) and miR-486 (p < 0.001). Expression of 3 miRNAs changed within the alemtuzumab group: miR-146 (p < 0.001), miR-155 (p < 0.001) and miR-31 (p < 0.001). Levels of IL-13, IL-4, IFN-γ, BAFF, IL-5, IL-9, IL-17F, IL-17A and IL-22 were different one year after transplantation compared to baseline. In no-induction group, concentration of sCD27, sB7.2 and sPD-L1 increased overtime. Expression of miR-23b, miR-146, miR-486, miR-155 and miR-31 was different in LTx recipients who received alemtuzumab compared to recipients without induction therapy. The observed cytokine pattern suggested proliferation of specific B cell subsets in alemtuzumab group and co-stimulation of T-cells in no-induction group.

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Section: Resultsmentioning

confidence: 99%

Differential expression of circulating miRNAs after alemtuzumab induction therapy in lung transplantation

Benazzo

Beigrezaei

Auner

et al. 2022

Sci Rep

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“…Functional pathway enrichment analysis was then performed on the prioritized target genes and the known pathways related to mmu-miR-155 cell-type-specific functions were among the top significantly enriched pathways ( Figure 3d ). For example, proliferative and apoptotic signaling pathways in B cells 40,41 , cytokine and co-stimulation related pathways in dendritic cells 42,43 , and activation and differentiation pathways in CD4+ T cells 44,45 . However, such enrichment was much weaker for the differentially expressed (logFC < 0 and FDR <= 0.05) miR-155 target genes (N=36, 110, 6 and 13).…”

Section: Resultsmentioning

confidence: 99%

Differential Regulation Analysis Quantifies Mirna Regulatory Roles and Context-Specific Targets

Ning

Spira

Beane

et al. 2022

Preprint

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Rewiring of transcriptional regulatory networks has been implicated in many biological and pathological processes. However, most current methods for detecting rewiring events (differential network connectivity) are not optimized for miRNA-mediated gene regulation and fail to systematically examine predicted target genes in study designs with multiple experimental or phenotypic groups. We developed a novel method to address these shortcomings. The method first estimates miRNA-gene expression correlations with Spatial Quantile Normalization to remove the mean-correlation relationship. Then, for each miRNA, genes are ranked by their correlation strength per experimental group. Enrichment patterns of predicted target genes are compared using the Anderson-Darling test and significance levels are estimated via permutation. Finally, context-specific target genes for each miRNA are identified with target prioritization based on the correlation strength between miRNA and predicted target genes within each group. In miR-155 KO RNA-seq data from four mice immune cell types, our method captures the known cell-specific regulatory differences of miR-155, and prioritized targets are involved in functional pathways with cell-type specificity. Moreover, in TCGA BRCA data, our method identified subtype-specific targets that were uniquely altered by miRNA perturbations in cell lines of the same subtype. Our work provides a new approach to characterize miRNA-mediated gene regulatory network rewiring across multiple groups from transcriptomic profiles. The method may offer novel insights into cell-type and cancer subtype-specific miRNA regulatory roles.

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“…Alterations in the expression of miRNAs could therefore be an important part of the pathophysiology of MS, since several studies have documented their relationship with immune system function. Among the most studied immune-related miRNAs are miR-155 and miR-146a; miR-155 induces CD8+ T‐cell activation, increases CD4+ T‐cell proliferation by regulating the expression of cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) and promotes dendritic cell maturation by suppressing c-Fos, SHIP1, KPC1 and SOCS1 proteins ( Chen et al, 2020 ), while miR-146a functions primarily as an immunosuppressant and acts as a negative regulator of myeloid cells and both CD4+ and CD8+ T lymphocytes, and promotes the function of Tregs ( Li et al, 2017 ).…”

Section: Micrornasmentioning

confidence: 99%

“…They found that miR-155 and miR-26a from PBMC of 24 RRMS patients treated with natalizumab and observed a decrease in the levels of these miRNAs during and after 6 months of treatment. miR-155 induced CD8+ T‐cell activation and increased CD4+ T‐cell proliferation ( Chen et al, 2020 ) while miR-26a induced Th-17 differentiation by altering the TGF-b signaling pathway ( Honardoost et al, 2014 ). Meira et al (2014) analyzed miR-126 expression only in CD4+ T lymphocytes from 24 natalizumab-treated RRMS patients, 12 patients with previously untreated RRMS, and 12 healthy controls.…”

Section: Micrornas and Disease Modifying Therapymentioning

confidence: 99%