Methyl-cpg-binding Domain Protein 2 Silencing Inhibits Th17 Differentiation of CD4+T cells Induced by Ovalbumin.
Iran J Immunol
; 20(1): 45-56, 2023 03 14.
Article
en En
| MEDLINE
| ID: mdl-36932919
ABSTRACT
Background:
Little is known about MBD2's epigenetic regulation in the immune pathogenesis of CD4+T cell differentiation.Objective:
This study attempted to explore the mechanism of methyl-cpg-binding domain protein 2 (MBD2) in CD4+T cell differentiation stimulated by environmental allergen ovalbumin (OVA).Methods:
Mononuclear cells were separated from the spleen tissues of male C57BL/6 mice. The OVA interfered with the differentiation of splenic mononuclear cells and CD4+T cells. The CD4+T cells were obtained by magnetic beads and identified by CD4 labeled antibody. CD4+T cells were transfected with lentivirus to silence MBD2 gene. A methylation quantification kit was used to detect 5-mC levels.Results:
The purity of CD4+T cells reached 95.99% after magnetic beads sorting. Treatment with 200 µg/mL OVA stimulated the CD4+T cells differentiation to Th17 cells and promoted the secretion of IL-17. After being induced, the Th17 cell ratio increased. 5-Aza inhibited the Th17 cell differentiation and the IL-17 level in a dose-dependent manner. Under the intervention of the Th17 induction and 5-Aza, MBD2 silencing inhibited the differentiation of Th17 cell, and decreased the IL-17 and 5-mC levels in the cell supernatants. MBD2 silencing reduced the scale of the Th17 cell and IL-17 levels in the OVA-treated CD4+T cells.Conclusion:
MBD2 affected IL-17 and 5-mC levels by mediating the Th17 cell differentiation in splenic CD4+T cells that were interfered with 5-Aza. OVA induced Th17 differentiation and increased IL-17 levels, inhibited by MBD2 silencing.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Interleucina-17
/
Proteínas de Unión al ADN
/
Células Th17
Límite:
Animals
Idioma:
En
Revista:
Iran J Immunol
Año:
2023
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
IR
/
IRAN
/
IRÃ