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KMID : 0624620210540100534
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BMB Reports
2021 Volume.54 No. 10 p.534 ~ p.539
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Entinostat, a histone deacetylase inhibitor, increases the population of IL-10+ regulatory B cells to suppress contact hypersensitivity
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Min Keun-Young
Lee Min-Bum
Hong Seong-Hwi
Lee Da-Jeong
Jo Min-Geun
Lee Ji-Eon
Choi Min-Yeong
You Jueng-Soo
Kim Young-Mi
Park Yeong-Min
Kim Hyuk-Soon
Choi Wahn-Soo
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Abstract
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IL-10+ regulatory B (Breg) cells play a vital role in regulating the immune responses in experimental autoimmune encephalomyelitis, colitis, and contact hypersensitivity (CHS). Several stimulants such as lipopolysaccharide (LPS), CD40 ligand, and IL-21 spur the activation and maturation of IL-10+ Breg cells, while the epigenetic mechanism for the IL-10 expression remains largely unknown. It is well accepted that the histone acetylation/ deacetylation is an important mechanism that regulates the expression of IL-10. We found that entinostat, an HDAC inhibitor, stimulated the induction of IL-10+ Breg cells by LPS in vitro and the formation of IL-10+ Breg cells to suppress CHS in vivo. We further demonstrated that entinostat inhibited HDAC1 from binding to the proximal region of the IL-10 expression promoter in splenic B cells, followed by an increase in the binding of NF-κB p65, eventually enhancing the expression of IL-10 in Breg cells.
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KEYWORD
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Contact hypersensitivity, Entinostat, Histone deacetylase inhibitor, Interleukin-10, Regulatory B cells
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