The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Highly purified Th17 cells from BDC2.5NOD mice convert into Th1-like cells in NOD/SCID recipient mice
Open accessAbstract
Th17 cells are involved in the pathogenesis of many autoimmune diseases, but it is not clear whether they play a pathogenic role in type 1 diabetes. Here we investigated whether mouse Th17 cells with specificity for an islet antigen can induce diabetes upon transfer into NOD/SCID recipient mice. Induction of diabetes in NOD/SCID mice via adoptive transfer of Th1 cells from BDC2.5 transgenic mice was prevented by treatment of the recipient mice with a neutralizing IFN-γ-specific antibody. This result suggested a major role of Th1 cells in the induction of disease in this model of type 1 diabetes. Nevertheless, transfer of highly purified Th17 cells from BDC2.5 transgenic mice caused diabetes in NOD/SCID recipients with similar rates of onset as in transfer of Th1 cells. However, treatment with neutralizing IL-17-specific antibodies did not prevent disease. Instead, the transferred Th17 cells, completely devoid of IFN-γ at the time of transfer, rapidly converted to secrete IFN-γ in the NOD/SCID recipients. Purified Th17 cells also upregulated Tbet and secreted IFN-γ upon exposure to IL-12 in vitro and in vivo in NOD/SCID recipients. These results indicate substantial plasticity of Th17 commitment toward a Th1-like profile.
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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Transforming growth factor-β induces development of the TH17 lineage
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Phenotypic and functional features of human Th17 cells
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Metadata
- Authors
- Bending, D., De La Peña, H., Veldhoen, M., Phillips, J. M., Uyttenhove, C., Stockinger, B., & Cooke, A.
- Venue
- Journal of Clinical Investigation
- Published
- 2009-03-02
- Volume
- 119
- Issue
- 3
- Pages
- 565-572
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2072449713
- Cited by
- 558
- References
- 7
- FWCI
- 30.68
- Type
- journal article
- Language
- en
- Open access
- green
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