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
MAPK regulation of gene expression in airway smooth muscle.
TL;DR: This review will focus on inflammatory and growth factor mediators of cell-cell signaling regulated by the ERK and p38 MAPK pathways in airway smooth muscle (ASM) that participate in pathological changes in ASM that accompany symptoms of asthma.
Journal ArticleDOI
The human IL-13 locus in neonatal CD4+ T cells is refractory to the acquisition of a repressive chromatin architecture.
TL;DR: The results suggest that differential IL-13 expression may depend on the acquisition of a permissive chromatin architecture at the proximal promoter in Th2 cells rather than the formation of locus-wide repressive chromatin in Th1 cells.
Journal ArticleDOI
Modulation of Th2 responses by peptide analogues in a murine model of allergic asthma: amelioration or deterioration of the disease process depends on the Th1 or Th2 skewing characteristics of the therapeutic peptide.
Edith M. Janssen,Antoon J. M. van Oosterhout,Annemiek J. M. L. van Rensen,Willem van Eden,Frans P. Nijkamp,Marca H. M. Wauben +5 more
TL;DR: The data show for the first time that a Th1-skewing peptide analogue of a dominant allergen epitope can modulate allerGEN-specific Th2 effector cells in an allergic response in vivo and suggest that the use of Th2-skeleton peptides instead of wild-type peptide may improve peptide immunotherapy and contribute to the development of a successful and safe immunotherapy for allergic patients.
Journal ArticleDOI
Late asthmatic reactions provoked by intradermal injection of T-cell peptide epitopes are not associated with bronchial mucosal infiltration of eosinophils or TH2-type cells or with elevated concentrations of histamine or eicosanoids in bronchoalveolar fluid
Brigitte M. Haselden,Mark Larché,Qiu Meng,Karen Shirley,Ryszard Dworski,Allen P. Kaplan,Christopher A. Bates,Douglas S. Robinson,Sun Ying,A. Barry Kay +9 more
TL;DR: Part of the asthma process might involve T cell-dependent airway narrowing with no requirement for IgE, mast cells, or infiltrating inflammatory cells.
Journal ArticleDOI
A Protective Role for C5a in the Development of Allergic Asthma Associated with Altered Levels of B7-H1 and B7-DC on Plasmacytoid Dendritic Cells
Xun Zhang,Ian P. Lewkowich,Gabriele Köhl,Jennifer R. Clark,Marsha Wills-Karp,Jörg Köhl,Jörg Köhl +6 more
TL;DR: C5a receptor (C 5aR)-targeting of C3aR-deficient mice during allergen sensitization not only reversed the protective effect but enhanced Th2 cytokine production, airway inflammation, and airway responsiveness, suggesting that the reduced allergic phenotype in C3AR- deficient mice results from protective C5aR signaling.
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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Journal ArticleDOI
Eosinophilic inflammation in asthma.
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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