期刊
IMMUNITY
卷 38, 期 6, 页码 1271-1284出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.05.011
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资金
- Academy of Finland [20122017, 140019, 256355]
- European Commission [EC-FP7-SYBILLA-201106]
- Sigrid Juselius Foundation
- Turku University Hospital Grant
- Biocenter Finland
- TISE Graduate School
- NIH [U01 ES017166]
- Ludwig Institute for Cancer Research
- WA State Life Sciences Discover Fund [265508]
- Academy of Finland (AKA) [140019, 256355, 140019, 256355] Funding Source: Academy of Finland (AKA)
Naive CD4(+) T cells can differentiate into specific helper and regulatory T cell lineages in order to combat infection and disease. The correct response to cytokines and a controlled balance of these populations is critical for the immune system and the avoidance of autoimmune disorders. To investigate how early cell-fate commitment is regulated, we generated the first human genome-wide maps of histone modifications that reveal enhancer elements after 72 hr of in vitro polarization toward T helper 1 (Th1) and T helper 2 (Th2) cell lineages. Our analysis indicated that even at this very early time point, cell-specific gene regulation and enhancers were at work directing lineage commitment. Further examination of lineage-specific enhancers identified transcription factors (TFs) with known and unknown T cell roles as putative drivers of lineage-specific gene expression. Lastly, an integrative analysis of immunopathogenic-associated SNPs suggests a role for distal regulatory elements in disease etiology.
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