PMID- 24836003
OWN - NLM
STAT- MEDLINE
DCOM- 20150123
LR  - 20211021
IS  - 1398-9995 (Electronic)
IS  - 0105-4538 (Linking)
VI  - 69
IP  - 7
DP  - 2014 Jul
TI  - LAPCs contribute to the pathogenesis of allergen-induced allergic airway 
      inflammation in mice.
PG  - 924-35
LID - 10.1111/all.12422 [doi]
AB  - BACKGROUND: The inflammatory immune response associated with allergic airway 
      inflammation in asthma involves T helper type 2 (Th2) immunity. Given the data 
      that a newly described late activator antigen-presenting cell (LAPC) population 
      promotes Th2 immunity in viral infections, we undertook studies to investigate 
      whether LAPCs have a pathogenic role in allergic airway inflammation. METHODS: We 
      employed acute ovalbumin (OVA) and house dust mite (HDM) sensitization and 
      challenge models to establish allergic airway inflammation in mice, followed by 
      the analysis of lungs and draining lymph node (DLN) cell infiltrates, 
      immunoglobulin E (IgE) production, and airway hyper-responsiveness (AHR). We 
      tested whether adoptive transfer of LAPCs isolated from mice with established 
      allergic airway inflammation augments the development of sensitization in naive 
      mice. RESULTS: We provide evidence that in both OVA and HDM mouse models of 
      allergic inflammation, LAPCs accumulate in the lungs and draining lymph nodes 
      (DLNs), concomitant with the onset of lung pathology, allergen-specific IgE 
      production, eosinophilia, and Th2 cytokine production. Adoptive transfer 
      experiments using OVA-activated LAPCs reveal exacerbation of disease pathology 
      with an increase in lung inflammatory cells, eosinophilia, circulating IgE, Th2 
      cytokine production, and a worsening of AHR. OVA-activated LAPCs preferentially 
      increased GATA-3 induction in naive CD4(+) T cells. CONCLUSIONS: Together, these 
      data suggest an important role for LAPCs in polarizing the Th2 response in mouse 
      models of allergic airway inflammation.
CI  - (c) 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Hawkshaw, C
AU  - Hawkshaw C
AD  - Toronto General Research Institute, University Health Network, Toronto, ON, 
      Canada; Department of Immunology, University of Toronto, Toronto, ON, Canada.
FAU - Scott, J A
AU  - Scott JA
FAU - Chow, C-W
AU  - Chow CW
FAU - Fish, E N
AU  - Fish EN
LA  - eng
GR  - 100714/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140517
PL  - Denmark
TA  - Allergy
JT  - Allergy
JID - 7804028
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Antigen-Presenting Cells/*immunology
MH  - Asthma/*immunology
MH  - Disease Models, Animal
MH  - Female
MH  - Flow Cytometry
MH  - Hypersensitivity/*immunology
MH  - Immunoglobulin E/immunology
MH  - Inflammation/*immunology
MH  - Lymphocyte Activation/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Ovalbumin/immunology
MH  - Pyroglyphidae/immunology
MH  - Th2 Cells/immunology
OTO - NOTNLM
OT  - Th2 immune response
OT  - allergic airway inflammation
OT  - late activator antigen-presenting cell
EDAT- 2014/05/20 06:00
MHDA- 2015/01/24 06:00
CRDT- 2014/05/20 06:00
PHST- 2014/04/01 00:00 [accepted]
PHST- 2014/05/20 06:00 [entrez]
PHST- 2014/05/20 06:00 [pubmed]
PHST- 2015/01/24 06:00 [medline]
AID - 10.1111/all.12422 [doi]
PST - ppublish
SO  - Allergy. 2014 Jul;69(7):924-35. doi: 10.1111/all.12422. Epub 2014 May 17.