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- W4313350088 abstract "Abstract Type 1 diabetes (T1D) is characterized by the destruction of insulin producing β-cells in the pancreas mediated by IFNγ+ T cells. Non-obese diabetic (NOD) mice and T1D patients share similar characteristics of disease progression and the immune defects associated with disease, e.g., their dendritic cells (DC) produce elevated levels of pro-inflammatory cytokines such as IL-12, a cytokine that drives differentiation of IFNγ+ T cells. We have identified a new defect in DC in NOD mice, i.e., an abnormal accumulation of the transcription factor, β-catenin, which appears to be associated with the production of pro-inflammatory cytokines. Moreover, we found that DC isolated from T1D patients also expressed elevated levels of β-catenin compared to healthy individuals. To examine the function of β-catenin in DC, we either transfected human or murine DC with β-catenin siRNA or cultured them with an β-catenin inhibitor, and found that the production of pro-inflammatory cytokines (IL-12, IL-6, TNF) and subsequent production of IFNγ by T cells added to the DC culture was abrogated. Finally, treatment of NOD mice with an β-catenin inhibitor delayed onset and decreased incidence of disease. These data suggest that elevated expression of β-catenin in T1D may regulate the pro-inflammatory cytokine production in DC that subsequently drives induction of β-cell destroying T cells. Manipulation of β-catenin may, therefore, be a novel strategy for preventing and/or treating T1D." @default.
- W4313350088 created "2023-01-06" @default.
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- W4313350088 date "2012-05-01" @default.
- W4313350088 modified "2023-09-27" @default.
- W4313350088 title "Overexpression of β-catenin in dendritic cells from type 1 diabetes patients and NOD mice may drive induction of T cells involved in β-cells destruction (123.34)" @default.
- W4313350088 doi "https://doi.org/10.4049/jimmunol.188.supp.123.34" @default.
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