Abstract:
: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.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Chu F,Hu Y,Zhou Y,Guo M,Lu J,Zheng W,Xu H,Zhao J,Xu Ldoi
10.1111/cei.13067subject
Has Abstractpub_date
2018-02-01 00:00:00pages
166-179issue
2eissn
0009-9104issn
1365-2249journal_volume
191pub_type
杂志文章abstract::Autoimmune Addison's disease (AAD), or primary adrenocortical insufficiency, is a classical organ-specific autoimmune disease with 160 years of history. AAD is remarkably homogeneous with one major dominant self-antigen, the cytochrome P450 21-hydroxylase enzyme, which is targeted by both autoantibodies and autoreacti...
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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doi:10.1111/cei.12416
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
doi:
更新日期:1981-09-01 00:00:00
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
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pub_type: 历史文章,杂志文章
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pub_type: 杂志文章
doi:10.1111/j.1365-2249.2006.03199.x
更新日期:2006-11-01 00:00:00
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
doi:
更新日期:1978-06-01 00:00:00
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
doi:
更新日期:1988-07-01 00:00:00
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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