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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Biological Evolution
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Cytokines / metabolism
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Cytokines / physiology*
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Eosinophilia / etiology
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Eosinophilia / pathology
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Eosinophils / immunology
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Gene Expression Regulation
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Helminthiasis / immunology*
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Helminthiasis / physiopathology
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Humans
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Immunoglobulin E / immunology
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Interferon-gamma / physiology
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Interleukin-2 / physiology
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Mast Cells / immunology
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Mice
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T-Lymphocyte Subsets / immunology*
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T-Lymphocyte Subsets / metabolism
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T-Lymphocytes, Helper-Inducer / immunology*
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T-Lymphocytes, Helper-Inducer / metabolism
Substances
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Cytokines
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Interleukin-2
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Immunoglobulin E
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Interferon-gamma