The epigenetic control of stemness in CD8 + T cell fate commitment
Male
Mice, Knockout
[SDV]Life Sciences [q-bio]
Cell Differentiation
Histone-Lysine N-Methyltransferase
Methyltransferases
CD8-Positive T-Lymphocytes
Listeria monocytogenes
Methylation
Chromatin
Epigenesis, Genetic
3. Good health
[SDV] Life Sciences [q-bio]
Histones
Mice, Inbred C57BL
Mice
03 medical and health sciences
0302 clinical medicine
Animals
Female
Listeriosis
Gene Silencing
RNA, Messenger
Immunologic Memory
Cells, Cultured
DOI:
10.1126/science.aah6499
Publication Date:
2018-01-16T22:40:52Z
AUTHORS (9)
ABSTRACT
Epigenetic modulation of effector T cells
The epigenetic states and associated chromatin dynamics underlying the initiation and maintenance of memory and effector CD8
+
T cells are poorly understood. Pace
et al.
found that mice lacking the histone H3 lysine 9 methyltransferase Suv39h1 had markedly reduced antigen-specific effector CD8
+
T cell responses to
Listeria monocytogenes
infection (see the Perspective by Henning
et al.
). Instead, CD8
+
T cells in these mice were enriched for genes associated with naïve and memory signatures and showed enhanced memory potential and increased survival capacity. Thus, Suv39h1 marks chromatin through H3K9me3 deposition and silences memory and stem cell programs during the terminal differentiation of effector CD8
+
T cells.
Science
, this issue p.
177
; see also p.
163
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