PMID- 29038036
OWN - NLM
STAT- MEDLINE
DCOM- 20190318
LR  - 20191210
IS  - 1521-7035 (Electronic)
IS  - 1521-6616 (Linking)
VI  - 187
DP  - 2018 Feb
TI  - Overexpression of Notch ligand Delta-like-1 by dendritic cells enhances their 
      immunoregulatory capacity and exerts antiallergic effects on Th2-mediated 
      allergic asthma in mice.
PG  - 58-67
LID - S1521-6616(17)30420-5 [pii]
LID - 10.1016/j.clim.2017.10.005 [doi]
AB  - Dendritic cells (DCs) are professional antigen-presenting cells, and Notch ligand 
      Delta-like-1 (DLL1) on DCs was implicated in type 1T helper (Th1) 
      differentiation. In this study, we produced genetically engineered bone 
      marrow-derived DCs that expressed DLL1 (DLL1-DCs) by adenoviral transduction. 
      DLL1-DCs exerted a fully mature phenotype, and had positive effects on expression 
      levels of interleukin (IL)-12 and costimulatory molecules. Coculture of 
      allogeneic T cells with ovalbumin (OVA)-pulsed DLL1-DCs enhanced T cell 
      proliferative responses and promoted Th1 cell differentiation. Furthermore, 
      adoptive transfer of OVA-stimulated DLL1-DCs into asthmatic mice alleviated the 
      cardinal features of allergic asthma, including immunoglobulin E (IgE) 
      production, airway hyperresponsiveness (AHR), airway inflammation, and production 
      of Th2-type cytokines. Notably, enhanced levels of the Th1-biased IgG(2a) 
      response and interferon (IFN)-gamma production were observed in these mice. Taken 
      together, these data indicate that DLL1-DCs promoted Th1 cell development to 
      alter the Th1/Th2 ratio and ameliorate Th2-mediated allergic asthma in mice.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Lee, Chen-Chen
AU  - Lee CC
AD  - Department of Microbiology and Immunology, School of Medicine, China Medical 
      University, Taichung, Taiwan.
FAU - Lin, Chu-Lun
AU  - Lin CL
AD  - Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical 
      University, Taipei, Taiwan.
FAU - Leu, Sy-Jye
AU  - Leu SJ
AD  - Department of Microbiology and Immunology, School of Medicine, College of 
      Medicine, Taipei Medical University, Taipei, Taiwan.
FAU - Lee, Yueh-Lun
AU  - Lee YL
AD  - Department of Microbiology and Immunology, School of Medicine, College of 
      Medicine, Taipei Medical University, Taipei, Taiwan. Electronic address: 
      yllee@tmu.edu.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171014
PL  - United States
TA  - Clin Immunol
JT  - Clinical immunology (Orlando, Fla.)
JID - 100883537
RN  - 0 (Calcium-Binding Proteins)
RN  - 0 (Dlk1 protein, mouse)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 187348-17-0 (Interleukin-12)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Asthma/*immunology
MH  - Calcium-Binding Proteins
MH  - Cell Differentiation
MH  - Cell Proliferation
MH  - Dendritic Cells/*immunology
MH  - Down-Regulation
MH  - Female
MH  - Hypersensitivity/*immunology
MH  - Immunoglobulin E/immunology
MH  - Intercellular Signaling Peptides and Proteins/genetics/*immunology
MH  - Interleukin-12/immunology
MH  - Lymphocyte Activation
MH  - Mice
MH  - Ovalbumin
MH  - Th1 Cells/immunology
MH  - Th2 Cells/*immunology
OTO - NOTNLM
OT  - Adenovirus
OT  - Allergic asthma
OT  - Delta-like-1
OT  - Dendritic cells
OT  - Th1
OT  - Th2
EDAT- 2017/10/19 06:00
MHDA- 2019/03/19 06:00
CRDT- 2017/10/18 06:00
PHST- 2017/06/09 00:00 [received]
PHST- 2017/09/22 00:00 [revised]
PHST- 2017/10/12 00:00 [accepted]
PHST- 2017/10/19 06:00 [pubmed]
PHST- 2019/03/19 06:00 [medline]
PHST- 2017/10/18 06:00 [entrez]
AID - S1521-6616(17)30420-5 [pii]
AID - 10.1016/j.clim.2017.10.005 [doi]
PST - ppublish
SO  - Clin Immunol. 2018 Feb;187:58-67. doi: 10.1016/j.clim.2017.10.005. Epub 2017 Oct 
      14.