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Blood, 1 December 2000, Vol. 96, No. 12, pp. 3847-3856
IMMUNOBIOLOGY
Up-regulation of costimulatory/adhesion molecules by histone
deacetylase inhibitors in acute myeloid leukemia cells
Takahiro Maeda,
Masayuki Towatari,
Hiroshi Kosugi, and
Hidehiko Saito
From the First Department of Internal Medicine, Nagoya
University School of Medicine, Nagoya, Japan.
Histone deacetylase inhibitors (HDACIs) have been used to focus on
the effects of inducing gene expression through the acetylation of
histones which results in chromatin remodeling. The
study explored whether HDACIs could induce the expression of
costimulatory/adhesion molecules on acute myeloid leukemia (AML) cells,
thereby effectively inducing tumor immunity. The expression of CD80,
CD86, human leukocyte antigen (HLA)-DR, HLA-ABC, and intracellular
adhesion molecule-1 (ICAM-1) was tested in human AML cell lines after
the addition of HDACI, sodium butyrate (SB). Generally, increased
expression of CD86 was observed by SB treatment in a majority of cell
lines, and ICAM-1 was expressed in fewer cell lines. Essentially the same results were obtained using other HDACIs such as FR901228, trichostatin A, and trapoxin A. Quantitation of transcripts of CD86 accompanied with RNA synthesis inhibition assay and nuclear run-on
assay revealed that SB up-regulates the CD86 expression transcriptionally. Furthermore, chromatin immunoprecipitation experiments showed that HDACI treatment caused remarkable acetylation on histone H3 and H4 at CD86 promoter chromatin in vivo. In 30 clinical
AML samples, CD86 expression was significantly increased (P < .001) by SB treatment, and the expression of HLA-DR
and ICAM-1 was moderately increased (P < .05) by SB
treatment. Finally, the allogeneic mixed leukocyte reaction (allo-MLR)
against HL60 cells pretreated with SB was enhanced 4-fold compared with
allo-MLR obtained with non-treated HL60 cells. These results
suggest that the immunotherapeutic use of HDACIs may become a novel
tool for treatment of AML.
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