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Updated: Sep 6, 2025
12:08
Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro
Published on: November 15, 2024
626
LNCRNA XIST Inhibits miR-377-3p to Hinder Th17 Cell Differentiation through Upregulating ETS1
Chen Yao1, Chao Li2, Zhijia Liu2
1Beijing IROT Key Laboratory, The 8th Medical Center of Chinese PLA General Hospital, 100091 Beijing City, China.
Computational Intelligence and Neuroscience
|June 24, 2022
Summary
Long non-coding RNA XIST hinders T helper 17 cell differentiation by upregulating ETS1, impacting inflammatory diseases. This study reveals LINC-XIST
Area of Science:
- Immunology
- Molecular Biology
- Cellular Biology
Background:
- T helper 17 (Th17) cell differentiation is implicated in autoimmune diseases like rheumatoid arthritis and systemic lupus erythematosus.
- The role of long non-coding RNA XIST (LINC-XIST) in Th17 cell differentiation requires further investigation.
Purpose of the Study:
- To elucidate the function of LINC-XIST in the differentiation of Th17 cells.
- To investigate the molecular mechanisms underlying LINC-XIST's regulation of Th17 cell differentiation.
Main Methods:
- Isolation of naïve CD4+ T cells from human whole blood and culture under Th17 polarizing conditions.
- Quantitative PCR (qPCR) to measure LINC-XIST and miR-153-3p expression.
- Luciferase reporter assays to validate interactions between LINC-XIST, miR-153-3p, and ETS1.
- ELISA for IL-17 concentration, Western blot for ETS1 protein expression, and flow cytometry for Th17 cell frequency.
Main Results:
- LINC-XIST expression decreased while miR-153-3p expression increased during Th17 cell differentiation.
- Overexpression of LINC-XIST reduced IL-17 expression and Th17 cell frequency.
- LINC-XIST directly regulates miR-153-3p, which in turn targets ETS1; ETS1 negatively impacts IL-17 production and Th17 cell differentiation.
Conclusions:
- Long non-coding RNA XIST inhibits Th17 cell differentiation by upregulating ETS1.
- This regulatory axis involving LINC-XIST, miR-153-3p, and ETS1 offers potential therapeutic targets for Th17-mediated diseases.
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