MicroRNAs expression profile in CCR6+ regulatory T cells

Zhao, Juanjuan; Li, Yongju; Hu, Yan; Chen, Chao; Zhou, Ya; Tao, Yijin; Guo, Ming; Qin, Nalin; Lin, Xu

doi:10.7287/peerj.preprints.471v2

Cited by 3 publications

(6 citation statements)

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“…Furthermore, CCR6 + Tregs expressed distinct patterns of miRNAs compared with CCR6 − Tregs did. 29 In the present study, we extended these findings by demonstrating that miR-21 could regulate the proliferation ability of CCR6 + Tregs in tumor sites. Similarly, Garchow et al 16 found that miR-21 could regulate the proliferation of CD4 + T cells.…”

Section: Discussionsupporting

confidence: 70%

“…27,28 Similarly, our most recent work also showed that CCR6 + Tregs expressed distinct miRNA profile compared with their CCR6 − counterpart. 29 These findings might support the fact that miRNAs played critical roles in the regulation of the distinct subset of Tregs. However, the exact regulation mechanism of distinct miRNAs involved in the biological function of different Treg subsets remains largely unknown.…”

Section: Discussionmentioning

confidence: 66%

“…Finally, it should be pointed out that global miRNA expression analysis showed that CCR6 + Tregs highly expressed other miRNA molecules different from CCR6 − Tregs. 29 Therefore, the potential role of these miRNA family members, which did not investigated in the current study, in the suppressive function of CCR6 + Tregs still remains to be valuably explored in further studies.…”

Section: Levels Of Mir-21 (Supplementarymentioning

confidence: 84%

“…The relative expression of miR-21 was performed according to manufacturer's protocol as described previously. 29…”

Section: Realtime Pcrmentioning

confidence: 99%

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MiR‐21 controls in situ expansion of CCR6⁺ regulatory T cells through PTEN/AKT pathway in breast cancer

Wang

et al. 2015

Immunol Cell Biol

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Our recent evidence showed that prior expansion of CCR6(+) Foxp3(+) regulatory T cells (Tregs) was important for their dominant enrichment in tumor tissue, which was closely related to poor prognosis of breast cancer patients. However, the underlying regulation mechanism of expansion of CCR6(+) Tregs in situ remains largely unknown. In this study, we reported that miR-21 was highly expressed in CCR6(+) Tregs in tumor tissues from a murine breast cancer model. And silencing of miR-21 could significantly reduce the proliferation of CCR6(+) Tregs in vitro. Adoptive cell-transfer assay further showed that silencing of miR-21 could alter the enrichment of CCR6(+) Tregs in the tumor mass and endow effectively antitumor effect of CD8(+) T cells using a murine breast cancer model. Mechanistic evidence showed that silencing of miR-21 enhanced the expression of its target phosphatase and tensin homolog deleted on chromosome ten (PTEN) and subsequently altered the activation of Akt pathway, which was ultimately responsible for reduced proliferation activity of CCR6(+) Tregs. Finally, we further revealed that miR-21 was also highly expressed on CCR6(+) Tregs in clinical breast cancer patients. Therefore, miR-21 can act as a fine tuner in the regulation of PTEN/Akt pathway transduction in the expansion of CCR6(+) Tregs in tumor sites and provided a novel insight into the development of therapeutic strategies for promoting T-cell immunity by regulating distinct subset of Tregs through targeting specific miRNAs.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 66%

Section: Levels Of Mir-21 (Supplementarymentioning

confidence: 84%

“…The relative expression of miR-21 was performed according to manufacturer's protocol as described previously. 29…”

Section: Realtime Pcrmentioning

confidence: 99%

See 2 more Smart Citations

MiR‐21 controls in situ expansion of CCR6⁺ regulatory T cells through PTEN/AKT pathway in breast cancer

Wang

et al. 2015

Immunol Cell Biol

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“…CD4 1 T cells are an important subpopulation of T cells which play a central role in innate immune responses, maintaining the balance of anti-inflammatory and proinflammatory responses, promoting activation of antigenpresenting cells (APCs) and B cells as well as promoting the accumulation of immune cells [33][34][35][36][37]. Increasing evidence demonstrates that the distinct miRNA molecule plays a critical regulatory role in the development and function of various immune cells, including CD4 1 T cells, which affect the pathogenesis and development of related clinical diseases [38][39][40][41][42][43][44]. For example, Zeng et al [45] reported that down-regulation of miR-451a affects the activation and proliferation of CD4 1 T cells by targeting the transcription factor myelocytomatosis oncogene (Myc) in dilated cardiomyopathy (DCM) patients, which contribute to the immunopathogenesis of DCM.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-126 deficiency enhanced the activation and function of CD4+T cells by elevating IRS-1 pathway

Chu

Zhou

et al. 2017

Clinical and Experimental Immunology

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Recent evidence has shown that microRNA-126 (miR-126) has been involved in the development and function of immune cells, which contributed to the pathogenesis of related clinical diseases. However, the potential role of miR-126 in the development and function of CD4 T cells remains largely unknown. Here we first found that the activation and proliferation, as well as the expression of interferon (IFN)-γ, of CD4 T cells from miR-126 knock-down (KD) mice using the miRNA-sponge technique were enhanced significantly in vitro, compared with those in CD4 T cells from wild-type (WT) mice. To monitor further the possible effect of miR-126 deficiency on the function of CD4 T cells in vivo, we used dextran sulphate sodium (DSS)-induced murine model of acute autoimmune colitis and found that miR-126 deficiency could elevate the pathology of colitis. Importantly, the proportion of CD4 T cells in splenocytes increased significantly in miR-126KD mice. Moreover, the expression levels of CD69 and CD44 on CD4 T cells increased significantly and the expression level of CD62L decreased significantly. Of note, adoptive cell transfer assay showed that the pathology of colitis was more serious in carboxyfluorescein succinimidyl ester (CFSE)-labelled miR-126KD CD4 T cell-transferred group, compared with that in the CFSE-labelled WT CD4 T cells transferred group. Consistently, the expression levels of CD69 and CD44 on CFSE cells increased significantly. Furthermore, both the proliferation and IFN-γ secretion of CFSE cells also increased significantly in the CFSE-labelled miR-126KD CD4 T cell-transferred group. Mechanistic evidence showed that the expression of insulin receptor substrate 1 (IRS-1), as a functional target of miR-126, was elevated in CD4 T cells from miR-126KD mice, accompanied by altered transduction of the extracellular regulated kinase, protein B (AKT) and nuclear factor kappa B (NF-κB) pathway. Our data revealed a novel role in which miR-126 was an intrinsic regulator in the function of CD4 T cells, which provided preliminary basis for exploring further the role of miR-126 in the development, function of CD4 T cells and related clinical diseases.

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MicroRNA‑30a controls the instability of inducible CD4+ Tregs through SOCS1

Zhou

et al. 2019

Mol Med Report

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inducible regulatory T cells (iTregs) are an important subset of Tregs and play a role in the maintenance of peripheral tolerance, and the occurrence of a number of diseases, including tumors and autoimmune diseases. However, the instability of iTregs is a major obstacle for their potential application in clinical trials. The underlying mechanism of iTreg instability remains largely unknown. in the present study, the expression level of microrna (mirna/mir)-30a in murine iTregs was evaluated using reverse transcription-quantitative Pcr. mir-30a mimics and a mir-negative control (nc) were transiently transfected into iTregs using nucleofector technology. The effects of mir-30a on the suppressive function of murine iTregs in vitro and in vivo were investigated using MTT, adoptive cell transfer (acT) and flow cytometry assays, as well as a murine model of lung cancer. In the present study, it was identified that the expression level of mir-30a was lower in murine iTregs in vitro compared with natural (n)Tregs. Furthermore, compared with mir-nc, mir-30a mimics impaired the suppressive function of murine iTregs on murine cd4 + T cell proliferation in vitro, which was accompanied by the altered expression of cytotoxic T lymphocyte-associated antigen 4 and glucocorticoid induced tumor necrosis factor receptor, as well as transforming growth factor-β and interleukin-10. it was also observed that, compared with mir-nc, mir-30a mimics abrogated the suppressive effects of murine iTregs on murine cd8 + T cell function in vivo, producing an effective antitumor effect in mice bearing 3ll lung cancer cells in the acT assay. From a mechanistic point, the expression level of suppressor of cytokine signaling 1, a putative target of mir-30a, was elevated, altering the activation of the akt and STaT1 pathway in the mir-30a mimic transfected group compared with the mir-nc group, reducing the suppressive function of murine iTregs. The present study identified a role for mir-30a in the instability of iTregs and provided a novel insight into the development of therapeutic strategies for promoting T-cell immunity via the regulation of iTreg instability by targeting specific miRNAs.

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MicroRNAs expression profile in CCR6+ regulatory T cells

Cited by 3 publications

References 0 publications

MiR‐21 controls in situ expansion of CCR6⁺ regulatory T cells through PTEN/AKT pathway in breast cancer

MiR‐21 controls in situ expansion of CCR6⁺ regulatory T cells through PTEN/AKT pathway in breast cancer

MicroRNA-126 deficiency enhanced the activation and function of CD4+T cells by elevating IRS-1 pathway

MicroRNA‑30a controls the instability of inducible CD4+ Tregs through SOCS1

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MicroRNAs expression profile in CCR6+ regulatory T cells

Cited by 3 publications

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MiR‐21 controls in situ expansion of CCR6+ regulatory T cells through PTEN/AKT pathway in breast cancer

MiR‐21 controls in situ expansion of CCR6+ regulatory T cells through PTEN/AKT pathway in breast cancer

MicroRNA-126 deficiency enhanced the activation and function of CD4+T cells by elevating IRS-1 pathway

MicroRNA‑30a controls the instability of inducible CD4+ Tregs through SOCS1

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MiR‐21 controls in situ expansion of CCR6⁺ regulatory T cells through PTEN/AKT pathway in breast cancer

MiR‐21 controls in situ expansion of CCR6⁺ regulatory T cells through PTEN/AKT pathway in breast cancer