Abstract
The immunological hallmarks of infection with parasitic belmintbs, namely eosinophilia, mastocytosis and increased IgE synthesis, all appear to be induced by cytokines from the T H2 subset of CD4 + T cells: IgE production is stimulated by interleukin 4 (IL-4), eosinophilia by IL-5 and mastocytosis by IL-3 and IL-4. Here, Fred Finkelman and colleagues argue that the functional significance of the eosinophilia-mastocytosis-IgE axis in helminth infection is unclear and suggest that in some worm infections T H2-cell cytokines may contribute to host protection, while in others they may promote parasite survival.
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