Abstract

The immunological hallmarks of infection with parasitic helminths, namely eosinophilia, mastocytosis and increased IgE synthesis, all appear to be induced by cytokines from the TH2 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 TH2-cell cytokines may contribute to host protection, while in others they may promote parasite survival.

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