T Cells, Cytokines, IgE and Allergic Inflammation

On the basis of results obtained in our and in other labs it is now possible to affirm that B cells require different signals to be induced to IgE production. The first signal is delivered by the physical contact between T and B cells. Another important signal required for IgE synthesis is provided by the release of IL-4 by activated T cells. Other complementary signals can potentiate IgE synthesis. On the other hand, an inhibitory activity on IgE production is exerted by IFN-γ, IFN-α and TGF-β. The existence of human T cells with stable Th1 and Th2 functional pattern has been recently documented. Moreover, the importance of Th2-like cells in the pathogenesis of atopic diseases has been stressed by two lines of evidence. The first line refers to the selection of Th2-like cells by allergens; the second line concerns the accumulation of Th2-like cells in target organs of atopic diseases. Some data suggest that atopic patients display an aberrant production in vitro of IL-4 and IL-5 even in response to antigens other than allergens. The results obtained by studying the possible influence of microenvironmental cytokines support the view that IL-4, IFN-γ, IFN-α and TGF-β play reciprocal regulatory effects on the development of human Th1 and Th2 clones. Our results as well as other recent immunobiological acquisitions have raised the possibility that T lymphocytes, particularly Th2-like cells can play a central role in the pathogenesis of allergic inflammation. Through the release of different combinations of cytokines this kind of cells can represent, much better than any other cell, a common factor linking IgE production, eosinophils, mast cells, basophils and macrophages.