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The inflammation of chronic asthma appears to be far more complex than a simple eosinophilic inflammation. All cells of the airways—inflammatory and structural—are involved and become activated including T cells, eosinophils, mast cells, macrophages, epithelial cells, fibroblasts, and even bronchial smooth muscle cells. All these cells play an effector role by the release of pro-inflammatory mediators,1 cytotoxic mediators, and cytokines resulting in vascular leakage, hypersecretion of mucus, smooth muscle contraction, epithelial shedding, and bronchial hyperresponsiveness. These cells are also involved in the regulation of inflammation of the airways and initiation of the process of remodelling by the release of cytokines and growth factors.
The cellular network in asthma
T lymphocytes play a central role in the development of airway inflammation.2 They are present in increased numbers in the airways of patients with fatal asthma3 or in patients with asthma of variable aetiology including occupational asthma.4 Most bear CD4 receptors while CD8 positive cells are more rarely identified, even during exacerbations of asthma.5 T cells are …
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