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- W2912209597 abstract "Oral lichen planus (OLP) is a T cell-mediated immune-related chronic disease, featured by accumulation of T cells and apoptosis of keratinocytes. Insulin-like growth factors 1 (IGF1) signaling, in combination with its downstream PI3K/AKT/MTOR cascade, plays pivotal roles in the regulation of inflammation and immune response. Meanwhile, TRB3 acts as a connective protein in the pathway. This study investigated the possible function of IGF1–PI3K/AKT/MTOR pathway in the local immunity of OLP. The expression of phosphorylated IGF1R (p-IGF1R) and TRB3 in lesional tissues of OLP was measured. The effects of T cells pretreated with PI3K inhibitor LY294002, MTOR antagonist rapamycin and exogenous IGF1 on the cell proliferation and apoptosis, as well as supernatant inflammatory cytokine levels were detected in co-culture system of activated T cells and oral keratinocytes, respectively. The expression of p-IGF1R and TRB3 in OLP lesions was significantly increased when compared with controls (P < 0.001). Rapamycin-treated T cells displayed enhanced apoptosis rate and promoted proliferation of their keratinocytes in the co-culture system. Notably, abnormal expression of IFN-γ and IL-4 were detected in supernatant of T cell alone and co-culture system in response to pharmacological modulators of IGF1–PI3K/MTOR pathway. The aberrant IGF1–PI3K/AKT/MTOR signaling may participate in the immunoregulatory mechanism of OLP, via regulation on the crosstalk between T cells and keratinocytes, as well as imbalanced cytokine networks." @default.
- W2912209597 created "2019-02-21" @default.
- W2912209597 creator A5007876335 @default.
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- W2912209597 date "2019-05-01" @default.
- W2912209597 modified "2023-10-10" @default.
- W2912209597 title "Aberrant IGF1–PI3K/AKT/MTOR signaling pathway regulates the local immunity of oral lichen planus" @default.
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- W2912209597 doi "https://doi.org/10.1016/j.imbio.2019.01.004" @default.
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