PMID- 24150243
OWN - NLM
STAT- MEDLINE
DCOM- 20141010
LR  - 20220321
IS  - 1460-2377 (Electronic)
IS  - 0953-8178 (Linking)
VI  - 26
IP  - 2
DP  - 2014 Feb
TI  - Th2-type inflammation instructs inflammatory dendritic cells to induce airway 
      hyperreactivity.
PG  - 103-14
LID - 10.1093/intimm/dxt047 [doi]
AB  - Dendritic cells (DCs) play critical roles in determining the fate of CD4(+) T 
      cells. Among DC sub-populations, monocyte-derived inflammatory DCs (iDCs) have 
      been shown to play an important role in the induction of adaptive immune 
      responses under inflammatory conditions. Although previous studies have shown 
      that DCs have an indispensable role in the induction of allergic airway 
      inflammation and airway hyperreactivity (AHR) in murine asthma models, the 
      precise roles of iDCs in the asthmatic responses remain largely unknown. We show 
      here that T(h)2 cell-mediated inflammation in murine asthma models induces the 
      expression of some markers of alternatively activated macrophage such as arginase 
      1 and resistin-like molecule-alpha in iDCs by a mechanism depending on the intrinsic 
      expression of STAT6. In contrast, T(h)1 cell-mediated inflammation induces iDCs 
      to express TNF-alpha and inducible nitric oxide synthase (iNOS), markers of TNF-alpha- 
      and iNOS-producing DCs. Moreover, we show that iDCs under a T(h)2 environment 
      play an important role in the induction of AHR, independently of allergic airway 
      inflammation. Our results thus indicate the importance of iDCs in the induction 
      of AHR as downstream effector cells in T(h)2 cell-mediated asthmatic responses.
FAU - Iwata, Arifumi
AU  - Iwata A
AD  - Department of Allergy and Clinical Immunology and.
FAU - Kawashima, Saki
AU  - Kawashima S
FAU - Kobayashi, Midori
AU  - Kobayashi M
FAU - Okubo, Ayako
AU  - Okubo A
FAU - Kawashima, Hirotoshi
AU  - Kawashima H
FAU - Suto, Akira
AU  - Suto A
FAU - Hirose, Koichi
AU  - Hirose K
FAU - Nakayama, Toshinori
AU  - Nakayama T
FAU - Nakajima, Hiroshi
AU  - Nakajima H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131022
PL  - England
TA  - Int Immunol
JT  - International immunology
JID - 8916182
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Retnla protein, mouse)
RN  - 0 (STAT6 Transcription Factor)
RN  - EC 3.5.3.1 (Arg1 protein, mouse)
RN  - EC 3.5.3.1 (Arginase)
SB  - IM
MH  - Animals
MH  - Arginase/metabolism
MH  - Asthma/*immunology
MH  - Bronchial Hyperreactivity/*immunology
MH  - Cells, Cultured
MH  - Cellular Microenvironment
MH  - Complement Pathway, Alternative
MH  - Dendritic Cells/*immunology
MH  - Disease Models, Animal
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/metabolism
MH  - Macrophages/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Pneumonia/immunology
MH  - STAT6 Transcription Factor/genetics/metabolism
MH  - Th2 Cells/*immunology
OTO - NOTNLM
OT  - STAT6
OT  - arginase 1
OT  - asthma
OT  - inflammatory DC
EDAT- 2013/10/24 06:00
MHDA- 2014/10/11 06:00
CRDT- 2013/10/24 06:00
PHST- 2013/10/24 06:00 [entrez]
PHST- 2013/10/24 06:00 [pubmed]
PHST- 2014/10/11 06:00 [medline]
AID - dxt047 [pii]
AID - 10.1093/intimm/dxt047 [doi]
PST - ppublish
SO  - Int Immunol. 2014 Feb;26(2):103-14. doi: 10.1093/intimm/dxt047. Epub 2013 Oct 22.