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Targeting interleukin-4 in asthma: lost in translation?

Tania Maes UGent, Guy Joos UGent and Guy Brusselle UGent (2012) AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY. 47(3). p.261-270
abstract
The first discovery that interleukin-4 (IL-4) is crucial in the development of allergic airway inflammation originates from the early 1990s. Whereas initial studies in experimental animal models provided the community with the optimistic view that targeting IL-4 would be the ultimate solution for treating asthma, the translation of these findings to the clinic has not been evident and has not yet fulfilled the expectations. Many technical challenges have been encountered in the attempts to modulate IL-4 expression or activity and in transferring knowledge of preclinical studies to clinical trials. Moreover, biological redundancies between IL-4 and IL-13 have compelled a simultaneous blockade of both cytokines. A number of phase I/II studies are now providing us with clinical evidence that targeting IL-4/IL-13 may provide some clinical benefit. However, the initial view that asthma is a purely Th2-mediated disease had to be revised. Currently, different asthma phenotypes have been described, implying that blocking specifically Th2 cytokines, such as IL-4, IL-5, and IL-13, should be targeted to only a specific subset of patients. Taking this into consideration, IL-4 (together with IL-13) deserves attention as subject of further investigations to treat asthma. In this review, we will address the role of IL-4 in asthma, describe IL-4 signaling, and give an overview of preclinical and clinical studies targeting the IL-4 Receptor pathway.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
asthma, asthma heterogeneity, Interleukin-4, allergy, targeted therapy, murine models, ALLERGIC AIRWAY INFLAMMATION, SOLUBLE IL-4 RECEPTOR, HUMAN LUNG FIBROBLASTS, ATOPIC ASTHMA, IN-VIVO, BRONCHIAL BIOPSIES, EPITHELIAL-CELLS, MESSENGER-RNA, MURINE MODEL, BRONCHOALVEOLAR LAVAGE
journal title
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
Am. J. Respir. Cell Mol. Biol.
volume
47
issue
3
pages
261 - 270
Web of Science type
Review
Web of Science id
000314404400001
JCR category
RESPIRATORY SYSTEM
JCR impact factor
4.148 (2012)
JCR rank
7/50 (2012)
JCR quartile
1 (2012)
ISSN
1044-1549
DOI
10.1165/rcmb.2012-0080TR
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2964188
handle
http://hdl.handle.net/1854/LU-2964188
date created
2012-07-25 11:40:10
date last changed
2013-07-08 13:54:11
@article{2964188,
  abstract     = {The first discovery that interleukin-4 (IL-4) is crucial in the development of allergic airway inflammation originates from the early 1990s. Whereas initial studies in experimental animal models provided the community with the optimistic view that targeting IL-4 would be the ultimate solution for treating asthma, the translation of these findings to the clinic has not been evident and has not yet fulfilled the expectations. Many technical challenges have been encountered in the attempts to modulate IL-4 expression or activity and in transferring knowledge of preclinical studies to clinical trials. Moreover, biological redundancies between IL-4 and IL-13 have compelled a simultaneous blockade of both cytokines. A number of phase I/II studies are now providing us with clinical evidence that targeting IL-4/IL-13 may provide some clinical benefit. However, the initial view that asthma is a purely Th2-mediated disease had to be revised. Currently, different asthma phenotypes have been described, implying that blocking specifically Th2 cytokines, such as IL-4, IL-5, and IL-13, should be targeted to only a specific subset of patients. Taking this into consideration, IL-4 (together with IL-13) deserves attention as subject of further investigations to treat asthma. In this review, we will address the role of IL-4 in asthma, describe IL-4 signaling, and give an overview of preclinical and clinical studies targeting the IL-4 Receptor pathway.},
  author       = {Maes, Tania and Joos, Guy and Brusselle, Guy},
  issn         = {1044-1549},
  journal      = {AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY},
  keyword      = {asthma,asthma heterogeneity,Interleukin-4,allergy,targeted therapy,murine models,ALLERGIC AIRWAY INFLAMMATION,SOLUBLE IL-4 RECEPTOR,HUMAN LUNG FIBROBLASTS,ATOPIC ASTHMA,IN-VIVO,BRONCHIAL BIOPSIES,EPITHELIAL-CELLS,MESSENGER-RNA,MURINE MODEL,BRONCHOALVEOLAR LAVAGE},
  language     = {eng},
  number       = {3},
  pages        = {261--270},
  title        = {Targeting interleukin-4 in asthma: lost in translation?},
  url          = {http://dx.doi.org/10.1165/rcmb.2012-0080TR},
  volume       = {47},
  year         = {2012},
}

Chicago
Maes, Tania, Guy Joos, and Guy Brusselle. 2012. “Targeting Interleukin-4 in Asthma: Lost in Translation?” American Journal of Respiratory Cell and Molecular Biology 47 (3): 261–270.
APA
Maes, Tania, Joos, G., & Brusselle, G. (2012). Targeting interleukin-4 in asthma: lost in translation? AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 47(3), 261–270.
Vancouver
1.
Maes T, Joos G, Brusselle G. Targeting interleukin-4 in asthma: lost in translation? AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY. 2012;47(3):261–70.
MLA
Maes, Tania, Guy Joos, and Guy Brusselle. “Targeting Interleukin-4 in Asthma: Lost in Translation?” AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 47.3 (2012): 261–270. Print.