Open AccessJournal Article
Interleukin-13: Central mediator of allergic asthma
Marsha Wills-Karp,Jackie Luyimbazi,Xueying Xu,Brian Schofield,Tamlyn Neben,Christopher L. Karp,Debra D. Donaldson +6 more
TLDR
In this article, the type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma.Abstract:
The worldwide incidence, morbidity, and mortality of allergic asthma are increasing. The pathophysiological features of allergic asthma are thought to result from the aberrant expansion of CD4 + T cells producing the type 2 cytokines interleukin-4 (IL-4) and IL-5, although a necessary role for these cytokines in allergic asthma has not been demonstrable. The type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma. IL-13 induces the pathophysiological features of asthma in a manner that is independent of immunoglobulin E and eosinophils. Thus, IL-13 is critical to allergen-induced asthma but operates through mechanisms other than those that are classically implicated in allergic responses.read more
Citations
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Journal ArticleDOI
Characterization of T cell subpopulations involved in the pathogenesis of asthma and allergic diseases.
Hans Yssel,Hervé Groux +1 more
TL;DR: A potential role of the subpopulation(s) of T regulatory cells in the induction and/or maintaince of the disease process will be discussed and the involvement of T lymphocyte subpopulations in the pathogenesis of allergic asthma and allergic diseases will be focused on.
Journal ArticleDOI
Differential regulation by glucocorticoid of interleukin-13-induced eosinophilia, hyperresponsiveness, and goblet cell hyperplasia in mouse airways.
Atsuko Kibe,Atsuko Kibe,Hiromasa Inoue,Hiromasa Inoue,Satoru Fukuyama,Satoru Fukuyama,Kentaro Machida,Kentaro Machida,Koichiro Matsumoto,Koichiro Matsumoto,Hiroshi Koto,Hiroshi Koto,Tomomi Ikegami,Tomomi Ikegami,Hisamichi Aizawa,Hisamichi Aizawa,Nobuyuki Hara,Nobuyuki Hara +17 more
TL;DR: It is suggested that glucocorticoid is not sufficient to suppress IL-13-induced AHR or goblet cell hyperplasia and that eotaxin expression and eosinophilic inflammation do not have a causal relationship to the induction of AHR, MUC5AC overexpression, or goblt cellhyperplasia induced by IL- 13.
Journal ArticleDOI
IL-13 mediates in vivo IL-9 activities on lung epithelial cells but not on hematopoietic cells
Valérie Steenwinckel,Jamila Louahed,Ciriana Orabona,Ciriana Orabona,François Huaux,Guy Warnier,Andrew N. J. McKenzie,Dominique Lison,Roy C. Levitt,Jean-Christophe Renauld +9 more
TL;DR: IL-9 can promote asthma through IL-13-independent pathways via expansion of mast cells, eosinophils, and B cells, and through induction of IL- 13 production by hemopoietic cells for mucus production and recruitment of eos inophils by lung epithelial cells.
Journal ArticleDOI
Eosinophilic esophagitis–linked calpain 14 is an IL-13–induced protease that mediates esophageal epithelial barrier impairment
Benjamin P. Davis,Emily M. Stucke,M. Eyad Khorki,Vladislav A. Litosh,Jeffrey K. Rymer,Mark Rochman,Jared Travers,Leah C. Kottyan,Marc E. Rothenberg +8 more
TL;DR: This work shows that recombinant CAPN14 cleaves a calpain-specific substrate and is inhibited by 4 classical calpain inhibitors: MDL-28170, acetyl-calpastatin, E-64, and PD151746, and shows a molecular and cellular pathway that contributes to T helper type 2 responses in mucosal epithelium.
Journal ArticleDOI
Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness
Hiromasa Inoue,Reiko Kato,Satoru Fukuyama,Atsushi Nonami,Kouji Taniguchi,Koichiro Matsumoto,Takako Nakano,Miyuki Tsuda,Mikiko Matsumura,Masato Kubo,Fumihiko Ishikawa,Byoung Gon Moon,Kiyoshi Takatsu,Yoichi Nakanishi,Akihiko Yoshimura +14 more
TL;DR: It is demonstrated that Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness, without affecting helper T cell differentiation, using Spred–deficient mice.
References
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Douglas S. Robinson,Qutayba Hamid,Sun Ying,Anne Tsicopoulos,J. Barkans,Andrew Bentley,Christopher Corrigan,Stephen R. Durham,A. B. Kay +8 more
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Jean Bousquet,Pascal Chanez,J.-Y. Lacoste,G. Barneon,N Ghavanian,I. Enander,Per Venge,Staffan Ahlstedt,J Simony-Lafontaine,P. Godard +9 more
TL;DR: Eosinophilic inflammation of the airways is correlated with the severity of asthma and these cells are likely to play a part in the epithelial damage seen in this disease.
Journal ArticleDOI
Requirement for IL-13 Independently of IL-4 in Experimental Asthma
Gabriele Grünig,Martha L. Warnock,Adil E. Wakil,Rajeev Venkayya,Frank Brombacher,Donna M. Rennick,Dean Sheppard,Markus Mohrs,Debra D. Donaldson,Richard M. Locksley,David B. Corry +10 more
TL;DR: This article showed that IL-4 receptor α chain-dependent pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL4 receptor and showed that selective neutralization of IL-13, a cytokine related to interleukin-4 that also binds to the α chain of the IL 4 receptor, ameliorated asthma phenotype.
Journal ArticleDOI
Cellular events in the bronchi in mild asthma and after bronchial provocation.
TL;DR: It is concluded that allergic asthma is accompanied by extensive inflammatory changes in the airways, even in mild clinical and subclinical disease.
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