FIGURE 1 | A central role for inflammatory TH2 cells in asthma.

From the following article:

Dendritic cells and epithelial cells: linking innate and adaptive immunity in asthma

Hamida Hammad & Bart N. Lambrecht

Nature Reviews Immunology 8, 193-204 (March 2008)

doi:10.1038/nri2275

Dendritic cells and epithelial cells: linking innate and adaptive immunity in asthma

Asthma is characterized by the infiltration of T helper 2 (TH2)-type cells, eosinophils, and mast cells (not shown) to the airway wall. The TH2-cell-associated cytokines interleukin-4 (IL-4), IL-5, IL-9, IL-13 and tumour-necrosis factor (TNF) have an important role in the pathogenesis of allergic asthma, as shown by their induction of most of the salient features of asthma, such as goblet-cell hyperplasia, airway-wall remodelling and bronchial hyper-reactivity. TH2-cell-associated cytokines are known to induce changes in blood vessels that lead to the upregulation of intercellular adhesion molecule 1 (ICAM1) and vascular cell-adhesion molecule 1 (VCAM1). This leads to the recruitment of very late antigen 4 (VLA4)-expressing eosinophils into the airway wall. These factors also induce the survival and activation of eosinophils. In addition to the effects of TH2-cell-associated cytokines on airway pathology, IL-4 and IL-13 are responsible for promoting immunoglobulin class switching to the IgE heavy chain, allowing for the production of IgE by B cells, a feature of allergic asthma (not depicted). TH2-type cytokines lead to stimulation of the epithelial–mesenchymal tropic unit, thus stimulating collagen deposition.

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