In:
Annual Review of Immunology, Annual Reviews, Vol. 22, No. 1 ( 2004-04-01), p. 789-815
Abstract:
▪ Abstract When asthma is diagnosed, eosinophilic inflammation and airway remodeling are established in the bronchial airways and can no longer be separated as cause and effect because both processes contribute to persistence and progression of disease, despite anti-inflammatory therapy. Th2 cells are continually active in the airways, even when disease is quiescent. IL-13 is the key effector cytokine in asthma and stimulates airway fibrosis through the action of matrix metalloproteinases on TGF-β and promotes epithelial damage, mucus production, and eosinophilia. The production of IL-13 and other Th2 cytokines by non-T cells augments the inflammatory response. Inflammation is amplified by local responses of the epithelium, smooth muscle, and fibroblasts through the production of chemokines, cytokines, and proteases. Injured cells produce adenosine that enhances IL-13 production. We review human and animal data detailing the cellular and molecular interactions in established allergic asthma that promote persistent disease, amplify inflammation, and, in turn, cause disease progression.
Type of Medium:
Online Resource
ISSN:
0732-0582
,
1545-3278
DOI:
10.1146/immunol.2004.22.issue-1
DOI:
10.1146/annurev.immunol.22.012703.104716
Language:
English
Publisher:
Annual Reviews
Publication Date:
2004
detail.hit.zdb_id:
1470451-1
SSG:
12
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