TH2-type cytokines in asthma.

TH2-type cytokines, particularly interleukin-5, together with granulocyte-macrophage colony-stimulating factor and interleukin-3, orchestrate the eosinophil response in asthma. Eosinophils are believed to be prime proinflammatory effector cells causing bronchial damage, which in turn, leads to chronic asthma symptoms. Although many cells may secrete cytokines (e.g., mast cells, epithelial cells, macrophages), all of which influence eosinophil differentiation, survival, and function, the TH2-type T cell is seen as having a central role since it is capable of direct antigen recognition. The putative "driving" antigen for asthmatic inflammation may be allergen, although other antigens (e.g., viral, epithelial) are also possible candidates. Although T cells also influence the synthesis of IgE, IgE-mediated mechanisms are seen as playing a secondary role only in atopic subjects, where they may be responsible for acute, short-lived symptoms superimposed on the chronic, on-going cell-mediated inflammatory disease.