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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
MiR-155 contributes to Th17 cells differentiation in dextran sulfate sodium (DSS)-induced colitis mice via Jarid2
Meng Xu1, Dongmei Zuo1, Xingxing Liu1
1Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
MicroRNAs (miRNAs) play an important role in regulating immune system function by mRNA destabilisation or inhibition of translation. Recently, miR-155 was detected to be significantly up-regulated in colonic tissues of patients with active UC. However, it is unknown whether miR-155 is involved in the pathogenesis of UC and how it influences immune response in dextran sulfate sodium (DSS)-induced colitis mice. Here, we investigated the role of miR-155 in UC. Firstly, through bioinformatics analysis and luciferase report assay, we found Jarid2 was a direct target of miR-155; then, we carried out in situ hybridization, immunofluorescence and flow cytometry, and revealed that miR-155 levels were increased, Jarid2 levels were decreased and the frequency of Th17 cells was elevated in DSS-induced mice; we also used lentiviral vector to deliver miR-155 inhibition sequences to silence miR-155 that was effectively taken up by epithelial cells. MiR-155 inhibition attenuated DSS-induced colonic damage and inhibited Th17 cells differentiation. This study suggests that miR-155 plays a host-damaging role during DSS-induced colitis mice and induces Th17 differentiation by targeting Jarid2.
Insights
MicroRNA-155 (miR-155) exacerbates inflammatory bowel disease by promoting Th17 cell differentiation. Inhibiting miR-155 in dextran sulfate sodium-induced colitis models reduced colonic damage and Th17 cell frequency.
Area of Science:
- Immunology
- Molecular Biology
- Gastroenterology
Background:
- MicroRNAs (miRNAs) regulate immune responses via mRNA destabilization or translational inhibition.
- Elevated miR-155 levels are observed in active ulcerative colitis (UC) colonic tissues.
- The specific role of miR-155 in UC pathogenesis and its influence on immune responses in dextran sulfate sodium (DSS)-induced colitis remain unclear.
Purpose of the Study:
- To investigate the role of miR-155 in the pathogenesis of UC.
- To elucidate the mechanism by which miR-155 influences immune responses in DSS-induced colitis.
- To identify direct targets of miR-155 relevant to UC.
Main Methods:
- Bioinformatics analysis and luciferase reporter assays to identify miR-155 targets.
- In situ hybridization, immunofluorescence, and flow cytometry to assess molecular and cellular changes in DSS-induced colitis mice.
- Lentiviral vectors used to deliver miR-155 inhibition sequences for gene silencing in epithelial cells.
Main Results:
- Jarid2 was identified as a direct target of miR-155.
- DSS-induced colitis mice showed increased miR-155 and Th17 cell frequency, alongside decreased Jarid2 levels.
- Inhibition of miR-155 attenuated DSS-induced colonic damage and suppressed Th17 cell differentiation.
Conclusions:
- miR-155 plays a detrimental role in DSS-induced colitis.
- miR-155 promotes Th17 cell differentiation by targeting Jarid2.
- Targeting miR-155 may represent a therapeutic strategy for UC.
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