Upregulated Inhibits Inflammatory Response Induced by in Human Monocytes Derived Dendritic Cells Via Targeting P65 and BCL-10

Overview

Journal Ann Transl Med

Publisher AME Publishing Company

Date 2020 Feb 12

PMID 32042774

Citations 3

Authors

Ting-Ting Wei

Zhuo Cheng

Zhi-De Hu

Lin Zhou

Ren-Qian Zhong

Affiliations

Soon will be listed here.

Abstract

Background: () is one of the most common fungal pathogens causing superficial and systemic infections. The innate immune system is the first defense line against infection. , a multifunctional microRNA (miRNA), has been proved to be a crucial regulator in innate immune response against bacterial and virus. However, the biological function of in innate immune response against infection remains unknown.

Methods: The expression , as well as inflammatory factors [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)], in monocytes derived dendritic cells (DCs) during heat-killed infection was detected by quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR). The biological functions of were investigated with "gain- and loss-of-function" experiments. Potential targets of were identified by bioinformatics analysis, luciferase assay and western blot. Small interfering RNA (siRNA) was used to validate the function of target.

Results: increased the expression of and pro-inflammatory factors. induced by was depended on Dectin-1-spleen tyrosine kinase (Syk)/Raf-1-MAPK signaling pathway. Furthermore, suppressed the secretion of pro-inflammatory cytokines induced by by targeting NF-κB p65 and B cell leukemia/lymphoma 10 (BCL-10).

Conclusions: In conclusion, up-regulated acts as a negative feedback regulator in the innate immune response against infection.

Citing Articles

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MicroRNA‑155‑5p affects regulatory T cell activation and immunosuppressive function by targeting BCL10 in myasthenia gravis.

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miR-155: An Important Role in Inflammation Response.

Hu J, Huang S, Liu X, Zhang Y, Wei S, Hu X J Immunol Res. 2022; 2022:7437281.

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