4.7 Article

Epithelial cell-derived micro RNA-146a generates interleukin-10-producing monocytes to inhibit nasal allergy

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SCIENTIFIC REPORTS
卷 5, 期 -, 页码 -

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NATURE PUBLISHING GROUP
DOI: 10.1038/srep15937

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资金

  1. National Natural Science Grant of China [81200732, 81271054, 81420756, 81373176]
  2. innovation of science and Technology Commission of Shenzhen Municipality, International Collaboration Project [JCYJ20140418095735538, JCYJ20140411150916749, JCYJ20120613173913654, JCYJ20130329110735981, JCYJ20120613173233810, GJHZ20130408174112021]

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The aberrant immunity plays an important role in the pathogenesis of allergic diseases. Micro RNAs (miR) are involved in regulating the immunity in the body. This study aims to test a hypothesis that miR-146a induces the expression of interleukin (IL)-10 in monocytes (Mos). In this study, the levels of miR-146a were determined by real time RT-PCR. The IL-10(+) Mos were evaluated by flow cytometry. The miR-146a-laden exosomes were generated with RPMI2650 cells (an airway epithelial cell line). An allergic rhinitis mouse model was developed. The results showed that nasal epithelial cells expressed miR-146a, which was markedly lower in the nasal epithelial cells of patients with nasal allergy than that in healthy controls. Exposure to T helper (Th)2 cytokines suppressed the levels of miR-146a in the nasal epithelial cells. The nasal epithelial cell-derived miR-146a up regulated the expression of IL-10 in Mos. The inducible IL-10(+) Mos showed an immune suppressor effect on the activities of CD4(+) effector T cells and the Th2 polarization in a mouse model of allergic rhinitis. In summary, nasal epithelial cells express miR-146a, the latter is capable of inducing IL-10 expression in Mos, which suppress allergic reactions in the mouse nasal mucosa.

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