Abstract
We report that Th2 cell cultures generated using T cells or splenocytes from IL-13-deficient mice produce significantly reduced levels of IL-4, IL-5, and IL-10 compared with wild-type. In contrast, IL-4 and IL-5 production by mast cells stimulated in vitro with PMA, ionomycin, or IgE cross-linking are unaffected. In vitro Th2 cell differentiation cannot be rescued by the addition of exogenous factors, but in vivo antigen challenge and administration of IL-13 can increase Th2-like cytokine responses as can infection with the parasitic nematode Nippostrongylus brasiliensis. IL-13-deficient mice also have lower basal levels of serum IgE and biased antigen-specific immunoglobulin responses. Thus, IL-13 is an important regulator of Th2 commitment and may therefore play a central role in atopy and infectious diseases.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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B-Lymphocytes / metabolism
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CD4-Positive T-Lymphocytes / cytology
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Cell Differentiation
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Drug Resistance / genetics
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Gene Targeting / methods
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Immunization
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Immunoglobulin E / blood
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Interleukin-13 / deficiency*
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Interleukin-13 / genetics
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Interleukin-13 / physiology
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Interleukin-4 / biosynthesis
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Interleukin-5 / biosynthesis
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Mast Cells / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Mutagenesis, Insertional
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Nematode Infections / immunology
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Neomycin / pharmacology
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Phosphoglycerate Kinase / genetics
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Receptors, IgE / biosynthesis
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Recombinant Proteins / administration & dosage
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Recombinant Proteins / pharmacology
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Spleen / cytology
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Th2 Cells / cytology*
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Th2 Cells / drug effects
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Th2 Cells / metabolism
Substances
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Interleukin-13
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Interleukin-5
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Receptors, IgE
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Recombinant Proteins
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Interleukin-4
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Immunoglobulin E
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Phosphoglycerate Kinase
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Neomycin