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MBD2 Regulates Th17 Cell Differentiation and Experimental Severe Asthma by Affecting IRF4 Expression
- Source :
- Mediators of Inflammation, Vol 2017 (2017), Mediators of Inflammation
- Publication Year :
- 2017
- Publisher :
- Hindawi Limited, 2017.
-
Abstract
- Th17 cells and IL-17 participate in airway neutrophil infiltration characteristics in the pathogenesis of severe asthma. Methyl-CpG binding domain protein 2 (MBD2) expression increased in CD4+ T cells in peripheral blood samples of asthma patients. However, little is known about that epigenetic regulation of MBD2 in both immunological pathogenesis of experimental severe asthma and CD4+ T cell differentiation. Here, we established a neutrophil-predominant severe asthma model, which was characterized by airway hyperresponsiveness (AHR), BALF neutrophil granulocyte (NEU) increase, higher NEU and IL-17 protein levels, and more Th17 cell differentiation. In the model, MBD2 and IRF4 protein expression increased in the lung and spleen cells. Under overexpression or silencing of the MBD2 and IRF4 gene, the differentiation of Th17 cells and IL-17 secretion showed positive changes. IRF4 protein expression showed a positive change with overexpression or silencing of the MBD2 gene, whereas there was no significant difference in the expression of MBD2 under overexpression or silencing of the IRF4 gene. These data provide novel insights into epigenetic regulation of severe asthma.
- Subjects :
- 0301 basic medicine
Article Subject
Receptor, ErbB-2
Neutrophil granulocyte
Cellular differentiation
Immunology
Biology
Pathogenesis
Mice
03 medical and health sciences
medicine
lcsh:Pathology
Animals
Gene silencing
Secretion
Epigenetics
Receptor
Lung
Interleukin-17
Cell Biology
Immunohistochemistry
Asthma
respiratory tract diseases
DNA-Binding Proteins
Mice, Inbred C57BL
030104 developmental biology
medicine.anatomical_structure
Interferon Regulatory Factors
Th17 Cells
Female
Interleukin-4
Research Article
IRF4
lcsh:RB1-214
Subjects
Details
- Language :
- English
- ISSN :
- 14661861 and 09629351
- Volume :
- 2017
- Database :
- OpenAIRE
- Journal :
- Mediators of Inflammation
- Accession number :
- edsair.doi.dedup.....9526e806cb8415b10fd15d1b3a2f9cf9