First published August 3, 2015 - More info
Treg dysfunction is associated with a variety of inflammatory diseases. Treg populations are defined by expression of the oligomeric transcription factor FOXP3 and inability to produce IL-2, a cytokine required for T cell maintenance and survival. FOXP3 activity is regulated post-translationally by histone/protein acetyltransferases and histone/protein deacetylases (HDACs). Here, we determined that HDAC3 mediates both the development and function of the two main Treg subsets, thymus-derived Tregs and induced Tregs (iTregs). We determined that HDAC3 and FOXP3 physically interact and that HDAC3 expression markedly reduces
Liqing Wang, Yujie Liu, Rongxiang Han, Ulf H. Beier, Tricia R. Bhatti, Tatiana Akimova, Mark I. Greene, Scott W. Hiebert, Wayne W. Hancock
Original citation: J Clin Invest. 2015;125(3):1111–1123. doi:10.1172/JCI77088.
Citation for this corrigendum: J Clin Invest. 2015;125(8):3304. doi:10.1172/JCI83084.
The GEO accession number provided in Methods was incorrect. The correct sentence is below.
All original microarray data were deposited in the NCBI’s Gene Expression Omnibus (GEO GSE68991).
The authors regret the error.