Figure 4
From: HDAC10 deletion promotes Foxp3+ T-regulatory cell function
HDAC10 co-precipitates with Foxp3. (A, B) Whole-mouse-genome oligoarrays (GeneChip™ Mouse Gene 2.0 ST) of WT and HDAC10−/− Treg. (A) Overview of differential gene expression, with 212 (0.62%) increased and 117 (0.34%) decreased genes in HDAC10−/− compared to WT Treg, respectively (Student t-test, FDR < 0.1, 1.5-fold differences). (B) Selected differentially expressed genes of potential interest, with red indicating increased, and blue decreased gene expression in HDAC10−/− Treg relative WT Treg control. Data normalized to the average of WT Treg per row. (C) Quantitative PCR of WT and HDAC10−/− Treg confirms the granzyme B increase noted in the microarray studies (n = 2–6/group, Wilcoxon matched-pairs signed rank test). (D–F) Evaluation of Foxp3 and HDAC10 interaction through overexpression. 293 T cells were transfected with empty vector, Foxp3, myc-tagged HDAC10, and/or HA-tagged p300, and proteins were extracted, immunoprecipitated (IP) and immunoblotted (IB) as indicated. HDAC10 and Foxp3 are shown to bind via HDAC10 (D) and Foxp3 (E) pulldown. (F) Overexpression of HDAC10 diminishes Foxp3 K31 acetylation and p300 expression. Tubastatin A (Tub A) is a class IIb HDAC inhibitor targeting both HDAC6 and HDAC1029. (G,H) Immunoblot showing Foxp3 protein expression in HDAC10−/− and WT Treg. (G) representative and (H) quantitative data pooled from three independent experiments (Student t-test). (C,H) Data shown as median ± IQR.
