PMID- 27639599
OWN - NLM
STAT- MEDLINE
DCOM- 20171218
LR  - 20181113
IS  - 1096-1186 (Electronic)
IS  - 1043-6618 (Print)
IS  - 1043-6618 (Linking)
VI  - 113
IP  - Pt A
DP  - 2016 Nov
TI  - DLL4(+) dendritic cells: Key regulators of Notch Signaling in effector T cell 
      responses.
PG  - 449-457
LID - S1043-6618(16)30873-8 [pii]
LID - 10.1016/j.phrs.2016.09.001 [doi]
AB  - Dendritic cells (DCs) are critical regulators of adaptive immune responses. DCs 
      can elicit primary T cell responses at low DC:T cell ratios through their 
      expression of high levels of antigen-presenting molecules and costimulatory 
      molecules. DCs are important for induction of functionally diverse T cell subsets 
      such as CD4(+) T helper (Th)1 and Th17 cells and effector CD8(+) T cells able to 
      reside in epithelial tissues. Recent studies begin illuminating the underlying 
      mechanism by which DCs regulate specialized T cell subsets. DCs are composed of 
      subsets that differ in their phenotype, localization and function. DCs expressing 
      high levels of DLL4 (DLL4(+) DCs), which is a member of Notch ligand family, are 
      newly discovered cells that have greater ability than DLL4(-) DCs to promote the 
      generation of Th1 and Th17 CD4(+) T cells. DLL4 derived from DLL4(+) DCs is also 
      important for promoting the differentiation and expansion of effector CD8(+) T 
      cells. Experimental studies have demonstrated that selective deletion of DLL4 in 
      DCs causes impaired antitumor immunity. In contrast, blocking DLL4 leads to 
      dramatic reduction of inflammatory T cell responses and their-mediated tissue 
      damage. We will discuss emerging functional specialization within the DLL4(+) DC 
      compartment, DLL4(+) DC biology and the impact of pharmacological modulation of 
      DLL4 to control inflammatory disorders.
CI  - Copyright (c) 2016 Elsevier Ltd. All rights reserved.
FAU - Meng, Lijun
AU  - Meng L
AD  - Fels Institute for Cancer Research and Molecular Biology, Temple University, USA.
FAU - Hu, Shaoyan
AU  - Hu S
AD  - Department of Hematology, Children's Hospital, Soochow University, Suzhou, China.
FAU - Wang, Jian
AU  - Wang J
AD  - Department of Hematology, Children's Hospital, Soochow University, Suzhou, China.
FAU - He, Shan
AU  - He S
AD  - Fels Institute for Cancer Research and Molecular Biology, Temple University, USA.
FAU - Zhang, Yi
AU  - Zhang Y
AD  - Fels Institute for Cancer Research and Molecular Biology, Temple University, USA; 
      Department of Microbiology and Immunology, Temple University, USA. Electronic 
      address: yi.zhang@temple.edu.
LA  - eng
GR  - K23 CA178202/CA/NCI NIH HHS/United States
GR  - R01 AR061569/AR/NIAMS NIH HHS/United States
GR  - R01 CA172106/CA/NCI NIH HHS/United States
GR  - R01 HL127351/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
DEP - 20160914
PL  - Netherlands
TA  - Pharmacol Res
JT  - Pharmacological research
JID - 8907422
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (Receptors, Notch)
RN  - 0 (delta protein)
SB  - IM
MH  - Animals
MH  - Cell Differentiation/immunology
MH  - Dendritic Cells/*immunology
MH  - Humans
MH  - Inflammation/immunology
MH  - Intracellular Signaling Peptides and Proteins/immunology/*metabolism
MH  - Membrane Proteins/immunology/*metabolism
MH  - Receptors, Notch/immunology/*metabolism
MH  - Signal Transduction/immunology
MH  - T-Lymphocyte Subsets/*immunology
PMC - PMC5571445
MID - NIHMS819079
OTO - NOTNLM
OT  - Alloimmunity and autoimmunity
OT  - DLL4
OT  - DLL4(+) DCs
OT  - Notch signaling
OT  - Tumor immunity
COIS- Conflict of interest disclosure The authors declare that they have no conflicts 
      of interest in relation to this manuscript.
EDAT- 2016/10/21 06:00
MHDA- 2017/12/19 06:00
PMCR- 2017/11/01
CRDT- 2016/09/19 06:00
PHST- 2016/09/01 00:00 [received]
PHST- 2016/09/02 00:00 [accepted]
PHST- 2016/10/21 06:00 [pubmed]
PHST- 2017/12/19 06:00 [medline]
PHST- 2016/09/19 06:00 [entrez]
PHST- 2017/11/01 00:00 [pmc-release]
AID - S1043-6618(16)30873-8 [pii]
AID - 10.1016/j.phrs.2016.09.001 [doi]
PST - ppublish
SO  - Pharmacol Res. 2016 Nov;113(Pt A):449-457. doi: 10.1016/j.phrs.2016.09.001. Epub 
      2016 Sep 14.