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Natural Killer Cells Promote Fetal Development through the Secretion of Growth-Promoting Factors.

Abstract Natural killer (NK) cells are present in large populations at the maternal-fetal interface during early pregnancy. However, the role of NK cells in fetal growth is unclear. Here, we have identified a CD49a+Eomes+ subset of NK cells that secreted growth-promoting factors (GPFs), including pleiotrophin and osteoglycin, in both humans and mice. The crosstalk between HLA-G and ILT2 served as a stimulus for GPF-secreting function of this NK cell subset. Decreases in this GPF-secreting NK cell subset impaired fetal development, resulting in fetal growth restriction. The transcription factor Nfil3, but not T-bet, affected the function and the number of this decidual NK cell subset. Adoptive transfer of induced CD49a+Eomes+ NK cells reversed impaired fetal growth and rebuilt an appropriate local microenvironment. These findings reveal properties of NK cells in promoting fetal growth. In addition, this research proposes approaches for therapeutic administration of NK cells in order to reverse restricted nourishments within the uterine microenvironment during early pregnancy.
PMID
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Authors

Mayor MeshTerms

Adoptive Transfer

Keywords

aged pregnancy

decidual NK cells

fetal development

fetal growth restriction

growth-promoting factors

maternal-fetal interface

tissue-resident NK

Journal Title immunity
Publication Year Start




PMID- 29262349
OWN - NLM
STAT- MEDLINE
DCOM- 20171226
LR  - 20171226
IS  - 1097-4180 (Electronic)
IS  - 1074-7613 (Linking)
VI  - 47
IP  - 6
DP  - 2017 Dec 19
TI  - Natural Killer Cells Promote Fetal Development through the Secretion of
      Growth-Promoting Factors.
PG  - 1100-1113.e6
LID - S1074-7613(17)30519-8 [pii]
LID - 10.1016/j.immuni.2017.11.018 [doi]
AB  - Natural killer (NK) cells are present in large populations at the maternal-fetal 
      interface during early pregnancy. However, the role of NK cells in fetal growth
      is unclear. Here, we have identified a CD49a(+)Eomes(+) subset of NK cells that
      secreted growth-promoting factors (GPFs), including pleiotrophin and osteoglycin,
      in both humans and mice. The crosstalk between HLA-G and ILT2 served as a
      stimulus for GPF-secreting function of this NK cell subset. Decreases in this
      GPF-secreting NK cell subset impaired fetal development, resulting in fetal
      growth restriction. The transcription factor Nfil3, but not T-bet, affected the
      function and the number of this decidual NK cell subset. Adoptive transfer of
      induced CD49a(+)Eomes(+) NK cells reversed impaired fetal growth and rebuilt an
      appropriate local microenvironment. These findings reveal properties of NK cells 
      in promoting fetal growth. In addition, this research proposes approaches for
      therapeutic administration of NK cells in order to reverse restricted
      nourishments within the uterine microenvironment during early pregnancy.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Fu, Binqing
AU  - Fu B
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China.
FAU - Zhou, Yonggang
AU  - Zhou Y
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China.
FAU - Ni, Xiang
AU  - Ni X
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China.
FAU - Tong, Xianhong
AU  - Tong X
AD  - Anhui Provincial Hospital, Hefei, Anhui 230001, China.
FAU - Xu, Xiuxiu
AU  - Xu X
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China.
FAU - Dong, Zhongjun
AU  - Dong Z
AD  - School of Medicine, Tsinghua University, Beijing 100086, China.
FAU - Sun, Rui
AU  - Sun R
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China.
FAU - Tian, Zhigang
AU  - Tian Z
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China. Electronic address: [email protected]
FAU - Wei, Haiming
AU  - Wei H
AD  - Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic
      Disease, School of Life Science and Medical Center, University of Science and
      Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for
      Physical Sciences at Microscale, University of Science and Technology of China,
      Hefei, Anhui 230001, China. Electronic address: [email protected]
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Immunity
JT  - Immunity
JID - 9432918
RN  - 0 (Antigens, CD)
RN  - 0 (Basic-Leucine Zipper Transcription Factors)
RN  - 0 (Carrier Proteins)
RN  - 0 (Cytokines)
RN  - 0 (EOMES protein, human)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Integrin alpha1)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (LILRB1 protein, human)
RN  - 0 (Leukocyte Immunoglobulin-like Receptor B1)
RN  - 0 (NFIL3 protein, human)
RN  - 0 (OGN protein, human)
RN  - 0 (T-Box Domain Proteins)
RN  - 0 (T-box transcription factor TBX21)
RN  - 134034-50-7 (pleiotrophin)
SB  - IM
MH  - Abortion, Habitual/genetics/*immunology/pathology
MH  - *Adoptive Transfer
MH  - Adult
MH  - Animals
MH  - Antigens, CD/genetics/immunology
MH  - Basic-Leucine Zipper Transcription Factors/genetics/immunology
MH  - Carrier Proteins/genetics/immunology/*secretion
MH  - Cellular Microenvironment
MH  - Cytokines/genetics/immunology/*secretion
MH  - Decidua/immunology/pathology
MH  - Female
MH  - Fetal Development/*immunology
MH  - Fetal Growth Retardation/genetics/immunology/pathology/*prevention & control
MH  - Fetus
MH  - Gene Expression Regulation, Developmental
MH  - HLA-G Antigens/genetics/immunology
MH  - Humans
MH  - Integrin alpha1/genetics/immunology
MH  - Intercellular Signaling Peptides and Proteins/genetics/immunology/*secretion
MH  - Killer Cells, Natural/cytology/immunology/*transplantation
MH  - Leukocyte Immunoglobulin-like Receptor B1/genetics/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Pregnancy
MH  - Signal Transduction
MH  - T-Box Domain Proteins/genetics/immunology
OTO - NOTNLM
OT  - aged pregnancy
OT  - decidual NK cells
OT  - fetal development
OT  - fetal growth restriction
OT  - growth-promoting factors
OT  - maternal-fetal interface
OT  - tissue-resident NK
EDAT- 2017/12/21 06:00
MHDA- 2017/12/27 06:00
CRDT- 2017/12/21 06:00
PHST- 2017/04/04 00:00 [received]
PHST- 2017/09/01 00:00 [revised]
PHST- 2017/11/21 00:00 [accepted]
PHST- 2017/12/21 06:00 [entrez]
PHST- 2017/12/21 06:00 [pubmed]
PHST- 2017/12/27 06:00 [medline]
AID - S1074-7613(17)30519-8 [pii]
AID - 10.1016/j.immuni.2017.11.018 [doi]
PST - ppublish
SO  - Immunity. 2017 Dec 19;47(6):1100-1113.e6. doi: 10.1016/j.immuni.2017.11.018.