ArrayExpress Uploader0mouseHDAC6 knock outHDAC6 knock outHDAC6 knock outWild typeWild typeWild type8539arrayexpress_sid8Foxp3+ T-regulatory cells (Tregs) are key to immune homeostasis such that their diminished numbers or function can cause autoimmunity and...21444725/profile/8773/arrayexpressuploader16chromatincolitishistoneproteinDec.12, 2014Falsehdac6-and-hsp90-control-the-functions-of-foxp3-t-rhttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-27896E-GEOD-27896_A-AFFY-36HDAC6 and HSP90 control the functions of Foxp3+ T regulatory cellsNov.24, 2014Foxp3+ T-regulatory cells (Tregs) are key to immune homeostasis such that their diminished numbers or function can cause autoimmunity and allograft rejection. Foxp3+ Tregs express histone/protein deacetylases (HDACs) that regulate chromatin remodeling, gene expression and protein function. Pan-HDAC inhibitors developed for oncology enhance Treg production and suppression but have limited non-oncologic applications given their broad effects. We show, using HDAC6-deficient mice and WT mice treated with HDAC6-specific inhibitors, that HDAC6 inhibition promotes Treg suppressive activity in models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully MHC-incompatible cardiac allograft rejection. Many of the beneficial effects of HDAC6 targeting are also achieved by inhibition of the HDAC6-regulated protein, HSP90. Hence, selective targeting of a single HDAC isoform, HDAC6, or its downstream target, HSP90, can promote Treg-dependent suppression of autoimmunity and transplant rejection. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of HDAC6 knock out, compared to wild type (C57BL6) controlE-GEOD-27896http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-27896/samples/