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Prevention of type 1 diabetes through infection with an intestinal nematode parasite requires IL-10 in the absence of a Th2-type response.
- Source :
-
Mucosal Immunology (1933-0219) . Mar2013, Vol. 6 Issue 2, p297-308. 12p. - Publication Year :
- 2013
-
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. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 19330219
- Volume :
- 6
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Mucosal Immunology (1933-0219)
- Publication Type :
- Academic Journal
- Accession number :
- 85463728
- Full Text :
- https://doi.org/10.1038/mi.2012.71