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2000
Volume 25, Issue 10
  • ISSN: 1566-5240
  • E-ISSN: 1875-5666

Abstract

Background

Among Th lineages from naïve CD4+T cells, Th17 cells producing IL-17 are strongly related to the pathogenesis of neutrophilic asthma. Leptin is involved in inflammation and immunity. Little is known about MBD2's epigenetic regulation in CD4+T cell differentiation.

Objective

Our study is intended to delve into the mode by which MBD2 interacts with Leptin to govern Th17 cell differentiation.

Methods

CD4+T cells were harvested from the spleen tissue of C57BL/6 mice. Th17 cell differentiation was determined by flow cytometry, and ELISA measured IL-17. Western blot and RT-qPCR were employed to detect the expression of MBD2, Leptin and RORγt. CO-IP was utilized to assess the relationship between MBD2 and Leptin.

Results

Under the overexpression or silencing of the MBD2 and Leptin genes, the differentiation of Th17 cells, IL-17 secretion, and RORγt expression all manifested positive changes. Leptin expression showed a positive variance upon overexpression or silencing of the MBD2 gene; however, there was no significant disparity in the expression of MBD2 under the overexpression or silencing of the Leptin gene. MBD2 can interact directly with Leptin.

Conclusion

MBD2 is capable of inducing the differentiation of naïve CD4+T cells into Th17 cells by augmenting the expression of Leptin.

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  • Article Type:
    Research Article
Keyword(s): CD4+T Cell; IL-17; Leptin; MBD2; RORγt expression; Th17 Cell
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