PMID- 31545817
OWN - NLM
STAT- MEDLINE
DCOM- 20200310
LR  - 20200310
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 14
IP  - 9
DP  - 2019
TI  - Regulation of NF-kappaB- and STAT1-mediated plasmacytoid dendritic cell functions by 
      A20.
PG  - e0222697
LID - 10.1371/journal.pone.0222697 [doi]
LID - e0222697
AB  - Dendritic cells (DCs) are professional antigen presenting cells involved in the 
      induction of T cell-mediated adaptive immunity. Plasmacytoid DCs (pDCs) originate 
      from lymphoid precursors and produce type I interferons (IFNs) in response to 
      pathogens. A20 is considered as a negative regulator of toll-like receptor (TLR) 
      signaling pathways, in which Toxoplasma gondii- derived profilin (TgPRF) is a 
      TLR11/12 ligand recognised by DCs to stimulate their maturation/activation. 
      Little is known about contributions of A20 to changes in biological properties of 
      pDCs. The present study, therefore, explored whether pDC functions are influenced 
      by A20. To this end, bone marrow cells were isolated and cultured with Flt3L to 
      attain CD8DCs, CD11bDCs and pDCs and followed by challenge with TgPRP in the 
      presence or absence of A20 siRNA. Expression of maturation markers were analysed 
      by flow cytometry, and secretion of inflammatory cytokines by ELISA, cell 
      migration by a transwell migration assay and expression of signalling molecules 
      by western blotting. As a result, treatment with A20 siRNA enhanced activations 
      of IkappaB-alpha and STAT-1, leading to increases in expressions of maturation markers 
      and cytokine productions as well as migration of TgPRP-treated pDCs, while mature 
      CD11bDCs produced at higher levels of TNF-alpha and IL-6 only. In addition, functions 
      of CD8DCs remained unaltered following A20 silencing. The effects of A20 on pDC 
      maturation and activation were completely abolished by IKK inhibitor and 
      partially blunted by fludarabine. In conclusion, the inhibitory effects of A20 on 
      pDC functions are expected to affect the immune response in T. gondii infection.
FAU - Duy, Pham Ngoc
AU  - Duy PN
AD  - Faculty of Biotechnology, Vietnam National University of Agriculture, Trau Quy, 
      Gia Lam, Hanoi, Vietnam.
FAU - Thuy, Nguyen Thu
AU  - Thuy NT
AD  - Institute of Biomedicine and Pharmacy, Vietnam Military Medical University, Ha 
      Dong, Hanoi, Vietnam.
FAU - Trang, Bui Kieu
AU  - Trang BK
AD  - Institute of Genome Research, Vietnam Academy of Science and Technology, Cau 
      Giay, Hanoi, Vietnam.
FAU - Giang, Nguyen Hoang
AU  - Giang NH
AD  - Institute of Genome Research, Vietnam Academy of Science and Technology, Cau 
      Giay, Hanoi, Vietnam.
FAU - Van, Nguyen Thi Hong
AU  - Van NTH
AD  - Department of Genetics, Faculty of Biology, VNU University of Science, Thanh 
      Xuan, Hanoi, Vietnam.
FAU - Xuan, Nguyen Thi
AU  - Xuan NT
AUID- ORCID: 0000-0003-3494-5136
AD  - Institute of Genome Research, Vietnam Academy of Science and Technology, Cau 
      Giay, Hanoi, Vietnam.
AD  - Graduate University of Science and Technology, Vietnam Academy of Science and 
      Technology, Cau Giay, Ha Noi, Vietnam.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190923
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (NF-kappa B)
RN  - 0 (Profilins)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (Stat1 protein, mouse)
RN  - EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
RN  - EC 3.4.22.- (Tnfaip3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Dendritic Cells/drug effects/metabolism/*physiology
MH  - Flow Cytometry
MH  - Mice, Inbred BALB C
MH  - NF-kappa B/metabolism/*physiology
MH  - Profilins/pharmacology
MH  - STAT1 Transcription Factor/metabolism/*physiology
MH  - Signal Transduction
MH  - Toxoplasma/metabolism
MH  - Tumor Necrosis Factor alpha-Induced Protein 3/*physiology
PMC - PMC6756537
COIS- The authors have declared that no competing interests exist.
EDAT- 2019/09/24 06:00
MHDA- 2020/03/11 06:00
PMCR- 2019/09/23
CRDT- 2019/09/24 06:00
PHST- 2019/04/17 00:00 [received]
PHST- 2019/09/05 00:00 [accepted]
PHST- 2019/09/24 06:00 [entrez]
PHST- 2019/09/24 06:00 [pubmed]
PHST- 2020/03/11 06:00 [medline]
PHST- 2019/09/23 00:00 [pmc-release]
AID - PONE-D-19-10953 [pii]
AID - 10.1371/journal.pone.0222697 [doi]
PST - epublish
SO  - PLoS One. 2019 Sep 23;14(9):e0222697. doi: 10.1371/journal.pone.0222697. 
      eCollection 2019.