Regulation of Memory CD8+ T Cell Differentiation by MicroRNAs

Zhang, Zhen; Zhang, Chaoqi; Li, Feng; Zhang, Bin; Zhang, Yi

doi:10.1159/000491532

Cited by 19 publications

(14 citation statements)

References 88 publications

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“…Tsai et al (27) had reported that miR-155-deficient CD8 + T cells toward the development of memory cells. As CD8 + Tcm cells have been shown to confer superior immunity both in vitro and in vivo, it remains elusive whether manipulation of miR-155 expression in T cells may prove a useful way to generate preferential memory cells and lead to better immunotherapy (28). Recent study showed that the antitumor ability of CD8 + T has been limited by tumor-induced immunosuppression.…”

Section: Discussionmentioning

confidence: 99%

miR-143 Regulates Memory T Cell Differentiation by Reprogramming T Cell Metabolism

Zhang

et al. 2018

The Journal of Immunology

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MicroRNAs are an important regulator for T cell immune response. In this study, we aimed to identify microRNAs with the potential to regulate T cell differentiation. The influence of miR-143 on differentiation and function of CD8 T cells from healthy donors were detected, and it was found that miR-143 overexpression could significantly increase the differentiation of central memory T (Tcm) CD8 cells, decrease cell apoptosis, and increase proinflammatory cytokine secretion. Furthermore, the specific killing of HER2-CAR T cells against esophageal cancer cell line TE-7 was enhanced by miR-143 overexpression. Glucose transporter 1 (Glut-1) was identified as the critical target gene of miR-143 in the role of T cell regulation. By inhibition Glut-1, miR-143 inhibited glucose uptake and glycolysis in T cell to regulated T cell differentiation. Tcm cell populations were also suppressed in parallel with the downregulation of miR-143 in tumor tissues from 13 patients with esophagus cancer. IDO and its metabolite kynurenine in the tumor microenvironment were screened as an upstream regulator of miR-143. IDO small interfering RNA significantly increased the expression of miR-143 and Tcm cell population. In conclusion, our results show that miR-143 enhanced antitumor effects of T cell by promoting memory T cell differentiation and metabolism reprogramming through Glut-1. Our findings will encourage the development of new strategies targeting miR-143 in both cancer cells and T cells.

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Section: Discussionmentioning

confidence: 99%

miR-143 Regulates Memory T Cell Differentiation by Reprogramming T Cell Metabolism

Zhang

et al. 2018

The Journal of Immunology

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“…Lots of reviews have described the important role of miRNAs in adaptive immunity (Dooley et al, 2013; Marques et al, 2015; Mehta and Baltimore, 2016; Zhang et al, 2018). miRNAs play an essential role in B-cell development and function, and one example of such is miR-181a-5p (Georgantas et al, 2007; Jensen et al, 2013).…”

Section: Epigenetic Regulation Of Genetic Programs In Immune Cellsmentioning

confidence: 99%

Epigenetic Regulation in the Pathogenesis of Sjögren Syndrome and Rheumatoid Arthritis

et al. 2019

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Autoimmune rheumatic diseases, such as Sjögren syndrome (SS) and rheumatoid arthritis (RA), are characterized by chronic inflammation and autoimmunity, which cause joint tissue damage and destruction by triggering reduced mobility and debilitation in patients with these diseases. Initiation and maintenance of chronic inflammatory stages account for several mechanisms that involve immune cells as key players and the interaction of the immune cells with other tissues. Indeed, the overlapping of certain clinical and serologic manifestations between SS and RA may indicate that numerous immunologic-related mechanisms are involved in the physiopathology of both these diseases. It is widely accepted that epigenetic pathways play an essential role in the development and function of the immune system. Although many published studies have attempted to elucidate the relation between epigenetic modifications (e.g. DNA methylation, histone post-translational modifications, miRNAs) and autoimmune disorders, the contribution of epigenetic regulation to the pathogenesis of SS and RA is at present poorly understood. This review attempts to shed light from a critical point of view on the identification of the most relevant epigenetic mechanisms related to RA and SS by explaining intricate regulatory processes and phenotypic features of both autoimmune diseases. Moreover, we point out some epigenetic markers which can be used to monitor the inflammation status and the dysregulated immunity in SS and RA. Finally, we discuss the inconvenience of using epigenetic data obtained from bulk immune cell populations instead specific immune cell subpopulations.

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“…The role of mirnas in a variety of intracellular signaling processes, including those associated with tumors, has been verified (15,16). They are also involved in the regulation of gene expression at the transcriptional and post-transcriptional levels (17), and in the regulation of the cell cycle (18), cell proliferation (19,20), cell differentiation (21)…”

Section: Introductionmentioning

confidence: 98%

miR‑139‑5p enhances cisplatin sensitivity in non‑small cell lung cancer cells by inhibiting cell proliferation and promoting apoptosis via the targeting of Homeobox protein Hox‑B2

Bao

Liu

et al. 2020

Mol Med Rep

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The development of chemotherapeutic dug resistance hinders the clinical treatment of cancer. Micrornas (mirnas/mirs) have been revealed to serve essential roles in the drug resistance of numerous types of cancer. mir-139-5p was previously reported to be associated with cisplatin (ddP) sensitivity in human nasopharyngeal carcinoma cells and colorectal cancer cells. However, the effect and underlying mechanism of mir-139-5p in ddP sensitivity in non-small cell lung cancer (nSclc) cells has not yet been fully elucidated. in the present study, the expression of mir-139-5p and Homeobox protein Hox-B2 (HoXB2) in nSclc tissues was examined by reverse transcription-quantitative polymerase chain reaction (rT-qPcr) and western blotting. Subsequently, the effect of mir-139-5p on the ddP sensitivity of nSclc cells in vitro was investigated. cell proliferation was examined using a cell counting Kit-8 assay. Western blotting was used to evaluate the protein expression of HoXB2, phosphorylated (p)-Pi3K, p-aKT, caspase-3 and cleaved-caspase-3, and rT-qPcr was used to evaluate the expression of mir-139-5p, and the mrna expression levels of HoXB2, Pi3K, aKT and caspase-3. The apoptotic rate of the cells was detected using flow cytometry. miR-139-5p expression in NSCLC tissues was shown to be significantly lower compared with that in adjacent tissues. additionally, mir-139-5p increased cell apoptosis and inhibited nSclc cell proliferation induced by ddP in vitro via modulating the Pi3K/aKT/caspase-3 signaling pathway. Furthermore, HOXB2 was identified to be a target of mir-139-5p, and mir-139-5p was revealed to sensitize nSclc cells to ddP via the targeting of HoXB2. Taken together, the results of the present study demonstrated that regulating the expression of mir-139-5p could provide a novel approach to reverse ddP resistance and increase chemosensitivity in the treatment of nSclc.

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Regulation of Memory CD8+ T Cell Differentiation by MicroRNAs

Cited by 19 publications

References 88 publications

miR-143 Regulates Memory T Cell Differentiation by Reprogramming T Cell Metabolism

miR-143 Regulates Memory T Cell Differentiation by Reprogramming T Cell Metabolism

Epigenetic Regulation in the Pathogenesis of Sjögren Syndrome and Rheumatoid Arthritis

miR‑139‑5p enhances cisplatin sensitivity in non‑small cell lung cancer cells by inhibiting cell proliferation and promoting apoptosis via the targeting of Homeobox protein Hox‑B2

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