Abstract
Although IL-4 induces expulsion of the gastrointestinal nematode parasite, Nippostrongylus brasiliensis, from immunodeficient mice, this parasite is expelled normally by IL-4-deficient mice. This apparent paradox is explained by observations that IL-4 receptor alpha chain (IL-4Ralpha)-deficient mice and Stat6-deficient mice fail to expel N. brasiliensis, and a specific antagonist for IL-13, another activator of Stat6 through IL-4Ralpha, prevents worm expulsion. Thus, N. brasiliensis expulsion requires signaling via IL-4Ralpha and Stat6, and IL-13 may be more important than IL-4 as an inducer of the Stat6 signaling that leads to worm expulsion. Additional observations made in the course of these experiments demonstrate that Stat6 signaling is not required for IL-4 enhancement of IgG1 production and actually inhibits IL-4-induction of mucosal mastocytosis.
Publication types
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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.
MeSH terms
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Animals
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Antibodies, Helminth / biosynthesis
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Female
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Gastrointestinal Diseases / immunology*
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Gastrointestinal Diseases / parasitology
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Host-Parasite Interactions / immunology
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Interferon-gamma / biosynthesis
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Interleukin-13 / deficiency*
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Interleukin-13 / genetics
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Intestinal Mucosa / immunology
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Mastocytosis / immunology
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Mutant Strains
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Mice, Nude
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Nippostrongylus / immunology*
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Receptors, Interleukin-4 / deficiency*
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Receptors, Interleukin-4 / genetics
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STAT6 Transcription Factor
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Signal Transduction
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Strongylida Infections / immunology*
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Trans-Activators / deficiency*
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Trans-Activators / genetics
Substances
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Antibodies, Helminth
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Interleukin-13
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Receptors, Interleukin-4
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STAT6 Transcription Factor
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Stat6 protein, mouse
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Trans-Activators
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Interferon-gamma