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@ARTICLE{ScottBrowne:130536,
author = {J. P. Scott-Browne and I. F. López-Moyado and S. Trifari
and V. Wong and L. Chavez$^*$ and A. Rao and R. M. Pereira},
title = {{D}ynamic {C}hanges in {C}hromatin {A}ccessibility {O}ccur
in {CD}8(+) {T} {C}ells {R}esponding to {V}iral
{I}nfection.},
journal = {Immunity},
volume = {45},
number = {6},
issn = {1074-7613},
address = {[Cambridge, Mass.]},
publisher = {Cell Press},
reportid = {DKFZ-2017-05615},
pages = {1327 - 1340},
year = {2016},
abstract = {In response to acute infection, naive CD8(+) T cells
expand, differentiate into effector cells, and then contract
to a long-lived pool of memory cells after pathogen
clearance. During chronic infections or in tumors, CD8(+)
T cells acquire an 'exhausted' phenotype. Here we present
genome-wide comparisons of chromatin accessibility and gene
expression from endogenous CD8(+) T cells responding to
acute and chronic viral infection using ATAC-seq and RNA-seq
techniques. Acquisition of effector, memory, or exhausted
phenotypes was associated with stable changes in chromatin
accessibility away from the naive T cell state. Regions
differentially accessible between functional subsets
in vivo were enriched for binding sites of transcription
factors known to regulate these subsets, including E2A,
BATF, IRF4, T-bet, and TCF1. Exhaustion-specific accessible
regions were enriched for consensus binding sites for NFAT
and Nr4a family members, indicating that chronic stimulation
confers a unique accessibility profile on exhausted cells.},
keywords = {Chromatin (NLM Chemicals)},
cin = {B062},
ddc = {610},
cid = {I:(DE-He78)B062-20160331},
pnm = {312 - Functional and structural genomics (POF3-312)},
pid = {G:(DE-HGF)POF3-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:27939672},
pmc = {pmc:PMC5214519},
doi = {10.1016/j.immuni.2016.10.028},
url = {https://inrepo02.dkfz.de/record/130536},
}