Oral diseases · 2024
HSP90 Complex From OLP Lesion Induces T-Cell Polarization via Activation of Dendritic Cells.
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Pan Lei, Chen Junjun, Lai Yirao, Du Guanhuan, Wang Haiyan, Sun Lei, Tang Guoyao, Wang Yufeng
Аннотация
OBJECTIVES: To investigate the effects of the heat shock protein 90 (HSP90) complex from oral lichen planus (OLP) lesion tissues on dendritic cell (DC) activation and the polarization of naïve T cells.
METHODS: Expression of HSP90 in OLP lesions and healthy control (HC) mucosa was evaluated by single-cell RNA sequence, IHC, qRT-PCR, and immunoblotting. HSP90 complex was extracted by immunoprecipitation from oral mucosa as the agonist of DCs. Expression of IFN-α and MHC was detected by flow cytometry. After cocultured with pre-stimulated DCs, polarization of naïve T cells was investigated by cytokine analysis.
RESULTS: HSP90 was significantly higher in the lamina propria of OLP lesion and closely related to lymphocyte infiltration. HSP90 complex of OLP lesion activated DCs via TLR9 and increased their IFN-α secretion and MHC II expression. Pre-stimulated DCs increased the proportion of Th17 cells.
CONCLUSIONS: HSP90 complex isolated from OLP lesion activated TLR9/IFN-α of DCs and further promoted the polarization of naïve T cells toward Th17 immunity.
METHODS: Expression of HSP90 in OLP lesions and healthy control (HC) mucosa was evaluated by single-cell RNA sequence, IHC, qRT-PCR, and immunoblotting. HSP90 complex was extracted by immunoprecipitation from oral mucosa as the agonist of DCs. Expression of IFN-α and MHC was detected by flow cytometry. After cocultured with pre-stimulated DCs, polarization of naïve T cells was investigated by cytokine analysis.
RESULTS: HSP90 was significantly higher in the lamina propria of OLP lesion and closely related to lymphocyte infiltration. HSP90 complex of OLP lesion activated DCs via TLR9 and increased their IFN-α secretion and MHC II expression. Pre-stimulated DCs increased the proportion of Th17 cells.
CONCLUSIONS: HSP90 complex isolated from OLP lesion activated TLR9/IFN-α of DCs and further promoted the polarization of naïve T cells toward Th17 immunity.