[Cellular and molecular mechanisms of allergic respiratory tract inflammation]

Knowledge of the cellular and molecular aspects of allergic airway inflammation has increased greatly. It is now clear that the type of specific immune response is determined by the preferential activation of CD4+ T cell subsets which secrete defined patterns of cytokines, and it has been suggested that Th2-like cells, able to produce IL-4 and IL-5, but not IFN-gamma, play an important role in the induction and maintenance of allergic airway inflammation. It has been demonstrated, moreover, that mast cells can secrete cytokines which are analogous to those produced by Th2-like cells. It is thus possible that both mast cells and Th2-like cells are involved in the induction and maintenance of allergic airway inflammation. We review here the genetic and environmental factors predisposing to allergic respiratory diseases, especially those potentially favoring the development of Th2-like cells. Particular attention is paid to the possible role of the antigen presenting cells, HLA class II molecules, T cell repertoire, and microenvironmental cytokines. We also discuss the crucial role that IL-4 plays in the development of Th2-like cells from their precursors as well as hypotheses concerning the possible molecular alterations responsible for the overexpression of the IL-4 gene in atopic subjects. This new information certainly facilitates the planning of preventive and treatment tactics for bronchial asthma.