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Entinostat, a histone deacetylase inhibitor, increases the population of IL-10+ regulatory B cells to suppress contact hypersensitivity
Keun Young Min1 (Graduate student), Min Bum Lee1 (PhD), Seong Hwi Hong2 (Graduate student), Dajeong Lee1 (PhD), Min Geun Jo1 (Graduate student), Jieon Lee1 (Graduate student), Min Yeung Choi1 (Graduate student), Jueng Soo You2 (Professor), Young Mi Kim1 (Professor), Yeung Min Park1 (Professor), Hyuk Soon Kim3 (Professor), Wahn Soo Choi 1,* (Professor)
1 Department of Immunology College of Medicine, Kon kuk University,
2Department of Biochemistry College of Medicine, Konkuk University,
3Department of Preventive Pharmacy, College of Pharmacy, Duksung Women's University,
4Department of Biomedical Sciences, College of Natural Science and Department of Health Sciences, Dong-A University
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-kB p65, eventually enhancing the expression of IL-10 in Breg cells.
Abstract, Accepted Manuscript(in press) [Submitted on July 13, 2021, Accepted on August 29, 2021]
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