Ghent University Academic Bibliography

Advanced

An anti-inflammatory role for plasmacytoid dendritic cells in allergic airway inflammation

Mirjam Kool UGent, Menno van Nimwegen, Monique Willart, Femke Muskens, Louis Boon, Joost Smit, Anthony Coyle, Björn Clausen, Henk Hoogsteden, Bart Lambrecht UGent, et al. (2009) JOURNAL OF IMMUNOLOGY. 183(2). p.1074-1082
abstract
It was previously shown that administration of recombinant human Fms-like tyrosine kinase receptor-3 ligand (Flt3L) before allergen challenge of sensitized mice suppresses the cardinal features of asthma through unclear mechanisms. Here, we show that Flt3L dramatically alters the balance of conventional to plasmacytoid dendritic cells (pDCs) in the lung favoring the accumulation of pDCs. Selective removal of pDCs abolished the antiinflammatory effect of Flt3L, suggesting a regulatory role for these cells in ongoing asthmatic inflammation. In support, we found that immature pDCs are recruited to the lungs of allergen-challenged mice irrespective of Flt3L treatment. Selective removal of pDCs during allergen challenge enhanced airway inflammation, whereas adoptive transfer of cultured pDCs before allergen challenge suppressed inflammation. Experiments in which TLR9 agonist CpG motifs were administered in vitro or in vivo demonstrated that pDCs were antiinflammatory irrespective of their maturation state. These effects were mediated through programmed death-1/programmed death ligand 1 interactions, but not through ICOS ligand, IDO, or IFN-alpha. These findings suggest a specialized immunoregulatory role for pDCs in airway inflammation. Enhancing the antiinflammatory properties of pDCs could be employed as a novel strategy in asthma treatment.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
regulatory T-cells, 3-dioxygenase, CPG oligodeoxynucleotides, respiratory syncytial virus, mouse model, FLT3 ligand, lymph-nodes, In-Vivo, inhaled antigen, bonemarrow, indoleamine 2, REGULATORY T-CELLS, RESPIRATORY SYNCYTIAL VIRUS, MOUSE MODEL, FLT3 LIGAND, LYMPH-NODES, IN-VIVO, INDOLEAMINE 2, 3-DIOXYGENASE, INHALED ANTIGEN, BONE-MARROW, CPG OLIGODEOXYNUCLEOTIDES
journal title
JOURNAL OF IMMUNOLOGY
J. Immunol.
volume
183
issue
2
pages
1074 - 1082
Web of Science type
Article
Web of Science id
000267812600033
JCR category
IMMUNOLOGY
JCR impact factor
5.646 (2009)
JCR rank
18/126 (2009)
JCR quartile
1 (2009)
ISSN
0022-1767
DOI
10.4049/jimmunol.0900471
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
798036
handle
http://hdl.handle.net/1854/LU-798036
date created
2009-12-02 15:51:30
date last changed
2016-12-19 15:47:11
@article{798036,
  abstract     = {It was previously shown that administration of recombinant human Fms-like tyrosine kinase receptor-3 ligand (Flt3L) before allergen challenge of sensitized mice suppresses the cardinal features of asthma through unclear mechanisms. Here, we show that Flt3L dramatically alters the balance of conventional to plasmacytoid dendritic cells (pDCs) in the lung favoring the accumulation of pDCs. Selective removal of pDCs abolished the antiinflammatory effect of Flt3L, suggesting a regulatory role for these cells in ongoing asthmatic inflammation. In support, we found that immature pDCs are recruited to the lungs of allergen-challenged mice irrespective of Flt3L treatment. Selective removal of pDCs during allergen challenge enhanced airway inflammation, whereas adoptive transfer of cultured pDCs before allergen challenge suppressed inflammation. Experiments in which TLR9 agonist CpG motifs were administered in vitro or in vivo demonstrated that pDCs were antiinflammatory irrespective of their maturation state. These effects were mediated through programmed death-1/programmed death ligand 1 interactions, but not through ICOS ligand, IDO, or IFN-alpha. These findings suggest a specialized immunoregulatory role for pDCs in airway inflammation. Enhancing the antiinflammatory properties of pDCs could be employed as a novel strategy in asthma treatment.},
  author       = {Kool, Mirjam and van Nimwegen, Menno and Willart, Monique and Muskens, Femke and Boon, Louis and Smit, Joost and Coyle, Anthony and Clausen, Bj{\"o}rn and Hoogsteden, Henk and Lambrecht, Bart and Hammad, Hamida},
  issn         = {0022-1767},
  journal      = {JOURNAL OF IMMUNOLOGY},
  keyword      = {regulatory T-cells,3-dioxygenase,CPG oligodeoxynucleotides,respiratory syncytial virus,mouse model,FLT3 ligand,lymph-nodes,In-Vivo,inhaled antigen,bonemarrow,indoleamine 2,REGULATORY T-CELLS,RESPIRATORY SYNCYTIAL VIRUS,MOUSE MODEL,FLT3 LIGAND,LYMPH-NODES,IN-VIVO,INDOLEAMINE 2,3-DIOXYGENASE,INHALED ANTIGEN,BONE-MARROW,CPG OLIGODEOXYNUCLEOTIDES},
  language     = {eng},
  number       = {2},
  pages        = {1074--1082},
  title        = {An anti-inflammatory role for plasmacytoid dendritic cells in allergic airway inflammation},
  url          = {http://dx.doi.org/10.4049/jimmunol.0900471},
  volume       = {183},
  year         = {2009},
}

Chicago
Kool, Mirjam, Menno van Nimwegen, Monique Willart, Femke Muskens, Louis Boon, Joost Smit, Anthony Coyle, et al. 2009. “An Anti-inflammatory Role for Plasmacytoid Dendritic Cells in Allergic Airway Inflammation.” Journal of Immunology 183 (2): 1074–1082.
APA
Kool, Mirjam, van Nimwegen, M., Willart, M., Muskens, F., Boon, L., Smit, J., Coyle, A., et al. (2009). An anti-inflammatory role for plasmacytoid dendritic cells in allergic airway inflammation. JOURNAL OF IMMUNOLOGY, 183(2), 1074–1082.
Vancouver
1.
Kool M, van Nimwegen M, Willart M, Muskens F, Boon L, Smit J, et al. An anti-inflammatory role for plasmacytoid dendritic cells in allergic airway inflammation. JOURNAL OF IMMUNOLOGY. 2009;183(2):1074–82.
MLA
Kool, Mirjam, Menno van Nimwegen, Monique Willart, et al. “An Anti-inflammatory Role for Plasmacytoid Dendritic Cells in Allergic Airway Inflammation.” JOURNAL OF IMMUNOLOGY 183.2 (2009): 1074–1082. Print.