Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.

Memory type 1 T helper (T(H)1) cells are characterized by the stable expression of interferon (IFN)-γ as well as by the epigenetic imprinting of the IFNG locus. Among innate cells, NK cells play a crucial role in the defense against cytomegalovirus (CMV) and represent the main source of IFN-γ. Recen...

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Autores principales:	Merlin Luetke-Eversloh, Quirin Hammer, Pawel Durek, Karl Nordström, Gilles Gasparoni, Matthias Pink, Alf Hamann, Jörn Walter, Hyun-Dong Chang, Jun Dong, Chiara Romagnani
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/5711f71e102e44c6ba1ad1bdff4dd3db
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spelling	oai:doaj.org-article:5711f71e102e44c6ba1ad1bdff4dd3db2021-11-25T05:45:55ZHuman cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.1553-73661553-737410.1371/journal.ppat.1004441https://doaj.org/article/5711f71e102e44c6ba1ad1bdff4dd3db2014-10-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.1004441https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Memory type 1 T helper (T(H)1) cells are characterized by the stable expression of interferon (IFN)-γ as well as by the epigenetic imprinting of the IFNG locus. Among innate cells, NK cells play a crucial role in the defense against cytomegalovirus (CMV) and represent the main source of IFN-γ. Recently, it was shown that memory-like features can be observed in NK cell subsets after CMV infection. However, the molecular mechanisms underlying NK cell adaptive properties have not been completely defined. In the present study, we demonstrated that only NKG2Chi NK cells expanded in human CMV (HCMV) seropositive individuals underwent epigenetic remodeling of the IFNG conserved non-coding sequence (CNS) 1, similar to memory CD8(+) T cells or T(H)1 cells. The accessibility of the CNS1 was required to enhance IFN-γ transcriptional activity in response to NKG2C and 2B4 engagement, which led to consistent IFN-γ production in NKG2C(hi) NK cells. Thus, our data identify epigenetic imprinting of the IFNG locus as selective hallmark and crucial mechanism driving strong and stable IFN-γ expression in HCMV-specific NK cell expansions, providing a molecular basis for the regulation of adaptive features in innate cells.Merlin Luetke-EverslohQuirin HammerPawel DurekKarl NordströmGilles GasparoniMatthias PinkAlf HamannJörn WalterHyun-Dong ChangJun DongChiara RomagnaniPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 10, p e1004441 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Merlin Luetke-Eversloh Quirin Hammer Pawel Durek Karl Nordström Gilles Gasparoni Matthias Pink Alf Hamann Jörn Walter Hyun-Dong Chang Jun Dong Chiara Romagnani Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.
description	Memory type 1 T helper (T(H)1) cells are characterized by the stable expression of interferon (IFN)-γ as well as by the epigenetic imprinting of the IFNG locus. Among innate cells, NK cells play a crucial role in the defense against cytomegalovirus (CMV) and represent the main source of IFN-γ. Recently, it was shown that memory-like features can be observed in NK cell subsets after CMV infection. However, the molecular mechanisms underlying NK cell adaptive properties have not been completely defined. In the present study, we demonstrated that only NKG2Chi NK cells expanded in human CMV (HCMV) seropositive individuals underwent epigenetic remodeling of the IFNG conserved non-coding sequence (CNS) 1, similar to memory CD8(+) T cells or T(H)1 cells. The accessibility of the CNS1 was required to enhance IFN-γ transcriptional activity in response to NKG2C and 2B4 engagement, which led to consistent IFN-γ production in NKG2C(hi) NK cells. Thus, our data identify epigenetic imprinting of the IFNG locus as selective hallmark and crucial mechanism driving strong and stable IFN-γ expression in HCMV-specific NK cell expansions, providing a molecular basis for the regulation of adaptive features in innate cells.
format	article
author	Merlin Luetke-Eversloh Quirin Hammer Pawel Durek Karl Nordström Gilles Gasparoni Matthias Pink Alf Hamann Jörn Walter Hyun-Dong Chang Jun Dong Chiara Romagnani
author_facet	Merlin Luetke-Eversloh Quirin Hammer Pawel Durek Karl Nordström Gilles Gasparoni Matthias Pink Alf Hamann Jörn Walter Hyun-Dong Chang Jun Dong Chiara Romagnani
author_sort	Merlin Luetke-Eversloh
title	Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.
title_short	Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.
title_full	Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.
title_fullStr	Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.
title_full_unstemmed	Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.
title_sort	human cytomegalovirus drives epigenetic imprinting of the ifng locus in nkg2chi natural killer cells.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/5711f71e102e44c6ba1ad1bdff4dd3db
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Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.

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