Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

In order to identify Bcl11b-bound sites in Treg cells(WT) and Tn cells and to determine Bcl11n and Foxp3 peak overlaps, we performed Bcl11b and Foxp3 ChIP-seq on respective cell populations. In order to understand whether Bcl11b recruitment to it's target sites is dependent on Foxp3 we performed Bcl111b ChIP-Seq in Tfn cells(derived from Foxp3GFPKO mice). Finally, to ask whether genome-wide occupancy of Foxp3 is affected in the absence of Bcl11b, we performed Foxp3 ChIP-seq in Bcl11b-deficient Treg cells(KO Treg). Genome-wide Chromatin Immunoprecipitation followed by next generation sequencing (ChIP-seq) for each conditions (3 replicates for Bcl11b ChIP in wild type Treg, 3 replicates for Bcl11b ChIP in wild type Tn, 2 replicates for Foxp3 ChIP in wild type Treg, 2 replicates for Bcl11b ChIP in Tfn and 2 replicates for Foxp3 ChIP in Bcl11b KO Treg) was done using Illumina HiSeq 2500.