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• W2125380322 abstract "Abstract CD4+FOXP3+ regulatory T cells are essential for immune tolerance, and murine studies suggest that their dysfunction can lead to type 1 diabetes (T1D). Human studies assessing regulatory T cell dysfunction in T1D have relied on analysis of FOXP3-expressing cells. Recently, distinct subsets of CD4+FOXP3+ T cells with differing function were identified. Notably, CD45RA−CD25intFOXP3low T cells lack suppressive function and secrete the proinflammatory cytokine IL-17. Therefore, we evaluated whether the relative fractions of CD4+FOXP3+ subsets are altered in new-onset T1D subjects. We report that children with new-onset T1D have an increased proportion of CD45RA−CD25intFOXP3low cells that are not suppressive and secrete significantly more IL-17 than other FOXP3+ subsets. Moreover, these T1D subjects had a higher proportion of both CD4+ and CD8+ T cells that secrete IL-17. The bias toward IL-17–secreting T cells in T1D suggests a role for this proinflammatory cytokine in the pathogenesis of disease." @default.
• W2125380322 created "2016-06-24" @default.
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• W2125380322 date "2010-10-01" @default.
• W2125380322 modified "2023-10-16" @default.
• W2125380322 title "Cutting Edge: Increased IL-17–Secreting T Cells in Children with New-Onset Type 1 Diabetes" @default.
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• W2125380322 doi "https://doi.org/10.4049/jimmunol.1001860" @default.
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