Immunology of asthma
From a histopathological standpoint, the inflammation in allergic asthma involves the entire thickness of the airway. Findings include generalized edema, denudation of the epithelium, subbasement membrane thickening, and smooth muscle and mucous gland hyperthropy. This pocess begin when dendritic cells, a subset of antigen-presenting cells found in the lung tissue, process inhaled antigens and present them to T lymphocytes through the interaction of the receptor molecule CD28 on T cells and its ligand CD80 on dendritic cells. This interactions result in T lymphocyte development down the TH2 pathway. TH2 lymphocytes are characterized by release of a family of proinflammatory cytokines, including IL-3, IL-4, IL-5, IL-13, tumor necrosis factor-α (TNF-α), and granulocyte-macrophage colony-stimulating factor. These cytokines promote development, activation, and survival of eosinophils. In addition, IL-4, IL-5, IL-13 and TNF-α activate endothelial cell adhesion proteins, ICAM-1 and VCAM-1, which assist inflammatory cell movement from blood vessels into the airway. IL-4 and IL-13 are key stimuli of B cells for antigen-specific IgE production, which initiates the allergic cascade. as a whole, these complex immunological processes lead to the pathologic processes that characterize asthma.