ArticleJournal of asthma and allergy2025
Mechanism of miR-206 in Regulating KLF4 and Affecting Th17 Cell Differentiation in Neutrophil Asthma Inflammation.
Article in Journal of asthma and allergy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: This study explores the role of miR-206 and KLF4 in neutrophilic asthma, focusing on their interaction and the molecular mechanisms by which miR-206 regulates Th17 cell-mediated immune-inflammatory responses through KLF4. Methods: RT-qPCR and flow cytometry assessed miR-206, KLF4 mRNA, and Th17 cell levels in asthma patients and healthy controls. CD4+ T cells were transfected to overexpress or inhibit miR-206, and KLF4, IL-17, and Th17 cell ratios were analyzed using RT-qPCR, ELISA, and flow cytometry. Correlation analysis evaluated relationships between miR-206, KLF4, and Th17 cells. Results: Severe asthma patients showed reduced miR-206 and elevated KLF4 mRNA levels, with increased Th17 cells and IL-17. miR-206 downregulated KLF4, negatively correlating with KLF4, Th17 cells, and IL-17. KLF4 positively correlated with Th17 cells and IL-17. miR-206 suppressed Th17 differentiation and IL-17 production by modulating KLF4. Conclusion: miR-206 is downregulated in acute asthma and targets KLF4, inhibiting Th17 cell differentiation and IL-17 production. These findings highlight miR-206 as a potential therapeutic target for asthma through its anti-inflammatory effects mediated by KLF4 and Th17 regulation.
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