Abstract
Helminth infection can prevent type 1 diabetes (T1D); however, the regulatory mechanisms inhibiting disease remain largely undefined. In these studies, nonobese diabetic (NOD) IL-4(-/-) mice were infected with the strictly enteric nematode parasite, Heligmosomoides polygyrus. Short-term infection, 5-7 weeks of age, inhibited T1D onset, as late as 40 weeks of age. CD4(+) T-cell STAT6 phosphorylation was inhibited, while suppressed signal transducer and activator of transcription 1 phosphorylation was sustained, as were increases in FOXP3(-), CD4(+) T-cell interleukin (IL)-10 production. Blockade of IL-10 signaling in NOD-IL-4(-/-), but not in NOD, mice during this short interval abrogated protective effects resulting in pancreatic β-cell destruction and ultimately T1D. Transfer of CD4(+) T cells from H. polygyrus (Hp)-inoculated NOD IL-4(-/-) mice to NOD mice blocked the onset of T1D. These studies indicate that Hp infection induces non-T-regulatory cells to produce IL-10 independently of STAT6 signaling and that in this Th2-deficient environment IL-10 is essential for T1D inhibition.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Autoantigens / immunology
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / metabolism
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Cytokines / genetics
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Cytokines / immunology
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Diabetes Mellitus, Type 1 / immunology*
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Diabetes Mellitus, Type 1 / prevention & control*
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Female
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Gene Expression Regulation
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Insulin-Secreting Cells / pathology
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Interferon-gamma / immunology
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Interferon-gamma / metabolism
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Interleukin-10 / immunology*
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Interleukin-10 / metabolism
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Interleukin-4 / deficiency
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Intestines / parasitology*
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Islets of Langerhans / immunology
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Lymphoid Tissue / immunology
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Lymphoid Tissue / metabolism
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Mice
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Mice, Inbred NOD
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Mice, Knockout
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Nematospiroides dubius / immunology*
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Phenotype
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Phosphorylation
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Receptors, Interleukin-10 / antagonists & inhibitors
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STAT1 Transcription Factor / metabolism
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STAT6 Transcription Factor / metabolism
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Signal Transduction
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Strongylida Infections / immunology*
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Th1 Cells / immunology
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Th1 Cells / metabolism
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Th2 Cells / immunology*
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Th2 Cells / metabolism
Substances
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Autoantigens
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Cytokines
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Receptors, Interleukin-10
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STAT1 Transcription Factor
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STAT6 Transcription Factor
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Interleukin-10
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Interleukin-4
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Interferon-gamma