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Entinostat, a histone deacetylase inhibitor, increases the population of IL-10(+) regulatory B cells to suppress contact hypersensitivity

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 sti-mulants such as lipopolysaccharide (LPS), CD40 ligand, and IL-21 spur the activation and maturation of IL-10(...

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Detalles Bibliográficos
Autores principales: Min, Keun Young, Lee, Min Bum, Hong, Seong Hwi, Lee, Dajeong, Jo, Min Geun, Lee, Ji Eon, Choi, Min Yeong, You, Jueng Soo, Kim, Young Mi, Park, Yeong Min, Kim, Hyuk Soon, Choi, Wahn Soo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society for Biochemistry and Molecular Biology 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8560462/
https://www.ncbi.nlm.nih.gov/pubmed/34488930
http://dx.doi.org/10.5483/BMBRep.2021.54.10.092
Descripción
Sumario: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 sti-mulants 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.