T cells, cytokines, IgE and allergic airways inflammation.

Great progress in the knowledge of the cellular and molecular signals involved in IgE antibody synthesis and in the induction of allergic inflammation has been achieved. A great deal of data support the view that Th-2-like cells are the main type of cells required for IgE production and are able to orchestrate allergic tissue inflammation. In particular, a reciprocal role for IL-4 (positive)- and IFN-gamma (negative)-producing CD4+ Th cells in the regulation of human IgE synthesis has been proven. However, a physical membrane interaction between T and B cells is required for IL-4-dependent IgE synthesis. The analysis of cytokine production by allergen-specific T cells has demonstrated that the great majority of these cells, derived from the peripheral blood of atopic patients, express a Th-2/Th-0 phenotype. Furthermore, in atopic subjects, aberrant in vitro production of IL-4 and IL-5, even in response to bacterial antigens, is displayed by CD4+ T cell clones. There is a general consensus on the accumulation of Th-2-like cells at the level of the target tissues of allergic inflammation such as the respiratory mucosa during allergic rhinitis and asthma, and at the level of the skin during atopic dermatitis. Even in other forms of bronchial asthma (intrinsic and occupational asthma), particular subsets of T cells, able to produce IL-2 and IL-5 but not IL-4, may play an important role. A great effort on the characterization of the factors that may favor the development in atopics of Th cells into Th-2-like cells has been made.(ABSTRACT TRUNCATED AT 250 WORDS)