MicroRNA-142 Is Critical for the Homeostasis and Function of Type 1 Innate Lymphoid Cells.
Animals
Cell Line
Female
HEK293 Cells
Homeostasis
/ immunology
Humans
Immunity, Innate
/ immunology
Killer Cells, Natural
/ immunology
Lymphocytes
/ immunology
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
MicroRNAs
/ immunology
Muromegalovirus
/ immunology
NIH 3T3 Cells
Receptors, Interleukin-15
/ immunology
Signal Transduction
/ immunology
Suppressor of Cytokine Signaling Proteins
/ immunology
Transforming Growth Factor beta
/ immunology
IL-15
ILC1-like cells
NK cells
cytokine receptors
innate lymphoid cells
integrin
microRNA-142
murine cytomegalovirus
tissue resident
Journal
Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918
Informations de publication
Date de publication:
17 09 2019
17 09 2019
Historique:
received:
21
02
2018
revised:
16
05
2019
accepted:
20
06
2019
pubmed:
14
8
2019
medline:
18
12
2019
entrez:
13
8
2019
Statut:
ppublish
Résumé
Natural killer (NK) cells are cytotoxic type 1 innate lymphoid cells (ILCs) that defend against viruses and mediate anti-tumor responses, yet mechanisms controlling their development and function remain incompletely understood. We hypothesized that the abundantly expressed microRNA-142 (miR-142) is a critical regulator of type 1 ILC biology. Interleukin-15 (IL-15) signaling induced miR-142 expression, whereas global and ILC-specific miR-142-deficient mice exhibited a cell-intrinsic loss of NK cells. Death of NK cells resulted from diminished IL-15 receptor signaling within miR-142-deficient mice, likely via reduced suppressor of cytokine signaling-1 (Socs1) regulation by miR-142-5p. ILCs persisting in Mir142
Identifiants
pubmed: 31402259
pii: S1074-7613(19)30286-9
doi: 10.1016/j.immuni.2019.06.016
pmc: PMC6750984
mid: NIHMS1537077
pii:
doi:
Substances chimiques
MicroRNAs
0
Mirn142 microRNA, mouse
0
Receptors, Interleukin-15
0
Suppressor of Cytokine Signaling Proteins
0
Transforming Growth Factor beta
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
479-490.e6Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK103039
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA173878
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI125615
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA171963
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA205239
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007200
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI127752
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA101937
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE025884
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007088
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA143379
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL090775
Pays : United States
Organisme : NCI NIH HHS
ID : F32 CA200253
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI078994
Pays : United States
Organisme : NCI NIH HHS
ID : K08 CA197369
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA009547
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI102924
Pays : United States
Organisme : NIAID NIH HHS
ID : F30 AI129110
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI095542
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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