Abstract
Over the last 5 years, three major new findings were made regarding the mechanism of regulation of IgE and IgG subclass antibody formation. First, it was shown that IL-4 induces B cells to secrete IgE, murine IgG1 and human IgG4 and that IFN-γ and IL-2 inhibit this effect. Second, it was found that cloned murine T helper cells can be divided into two types: Th1, secreting IL-2 and IFN-γ; and Th2, secreting IL-4 and IL-5. Third, murine mast cells, like Th2, secrete IL-4 and IL-5 but not IL-2 and IFN-γ. Soon after these in vitro data were obtained, direct and indirect evidence was obtained demonstrating that IL-4 and IFN-γ also act antagonistically on IgE formation in vivo. Collectively, this new information is a major breakthrough and demonstrates the important role of lymphokines in determining the Ig isotype secreted by B cells, particularly IgE and certain IgG subclasses. However, many aspects of IgE and IgG subclass regulation are not yet resolved and in particular, it is not clear what is abnormal in the lymphokine-regulated IgE antibody formation in atopic patients.
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