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[E. Immunology] E-8
Entinostat suppresses contact hypersensitivity by inducing IL-
10+ regulatory B cells
Minseong Kang¹, Hyuk Soon Kim¹,²*
¹Department of Health Sciences, The Graduate of Dong-A University, Busan 49315, Korea, ²Department of
Biomedical Science, Dong-A University, Busan 49315, Korea
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.
