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Genome-wide 5-hydroxymethylcytosine (5hmC) profiling by hMeDIP-seq in primary human CD4+T-cells polarized towards Th1 and Th2 time-series

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NIAID Data Ecosystem2026-05-01 收录
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https://www.ncbi.nlm.nih.gov/sra/ERP015415
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Differentiation of CD4+T-cells into effector subsets is a critical component of the adaptive immune system and an incorrect response can lead to autoimmunity or immune deficiency. Cellular differentiation including T-cell differentiation is accompanied by large-scale epigenetic remodeling, including changes in DNA methylation at key regulators of T-cell differentiation. The TET family of enzymes were recently shown to be able to catalyse methylated cytosine (5mC) into 5-hydroxymethylcytosine (5hmC) enabling a pathway of active removal of DNA methylation. Here, we characterize 5hmC, 5mC and transcriptional dynamics during human CD4+T-cell polarisation in a time series approach and relate these changes to profiles in ex-vivo CD4+memory subsets. We observed large-scale remodelling during early CD4+T-cell differentiation which was predictive of subsequent changes during late time points, these changes were also related to disease associated regions which we show can act as functional regulatory elements. This dataset was designed to assess how 5-hydroxymethylcytosine (5hmC) changes over time during human CD4+T-cell polarization towards Th1 and Th2. We tested an early (1 day) and late (5 day) timepoint to distinguish between replication-independent (early) and replication-dependent (late) changes. When comparing the time-series profiles, we observed an early gain followed by a late loss of 5hmC suggesting active 5hmC remodelling precedes lineage specification in CD4+T-cells. This submission contains the data from genome-wide 5-hydroxymethylcytosine (5hmC) profiling by hMeDIP-seq in primary human CD4+T-cells polarized towards Th1 and Th2 time-series. This submission is part of series containing 5hmC and DNA methylation profiling of the same samples. See related experiments E-MTAB-4685, E-MTAB-4687, E-MTAB-4688, E-MTAB-4689.
创建时间:
2023-10-13
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