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Cell. 2016 Aug 11;166(4):977-990. doi: 10.1016/j.cell.2016.07.006. Epub 2016 Aug 4.

Memory of Inflammation in Regulatory T Cells.

Author information

1
Howard Hughes Medical Institute and Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
2
Computational Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
3
Computational Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. Electronic address: cleslie@cbio.mskcc.org.
4
Howard Hughes Medical Institute and Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA; Ludwig Center at Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. Electronic address: rudenska@mskcc.org.

Abstract

Eukaryotic cells can "remember" transient encounters with a wide range of stimuli, inducing lasting states of altered responsiveness. Regulatory T (Treg) cells are a specialized lineage of suppressive CD4 T cells that act as critical negative regulators of inflammation in various biological contexts. Treg cells exposed to inflammatory conditions acquire strongly enhanced suppressive function. Using inducible genetic tracing, we analyzed the long-term stability of activation-induced transcriptional, epigenomic, and functional changes in Treg cells. We found that the inflammation-experienced Treg cell population reversed many activation-induced changes and lost its enhanced suppressive function over time. The "memory-less" potentiation of Treg suppressor function may help avoid a state of generalized immunosuppression that could otherwise result from repeated activation.

PMID:
27499023
PMCID:
PMC4996371
DOI:
10.1016/j.cell.2016.07.006
[Indexed for MEDLINE]
Free PMC Article

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