Abstract

Objectives The aim of this study was to screen the interacting proteins of TLR9 and to explore the function of TRIM21 overexpression. Study Design Buccal mucosal samples and peripheral blood mononuclear cells (PBMCs) were collected from both patients with oral lichen planus (OLP) and the healthy control group for the following studies: (1) co-immunoprecipitation (CoIP), followed by mass spectrometry, to screen for the interacting proteins of TLR9 in OLP lesions; (2) immunofluorescence colocalization analysis and plasmid transfection plus CoIP to verify protein interaction; (3) quantitative polymerase chain reaction (qPCR) to quantify its gene expression; immunohistochemistry to delineate its spatial distribution; (4) overexpression of this gene in T cells to test its function. Results (1) Of the 7 potential TLR9 interacting proteins predominantly present in OLP samples, TRIM21 was selected as the objective for further study; (2) immunofluorescence colocalization analysis and plasmid transfection plus CoIP were not able to verify the interaction between TRIM21 and TLR9; (3) significantly higher transcription of TRIM21 was revealed through qPCR; a larger amount of TRIM21 positive cells mainly infiltrated in the lamina propria of OLP lesions compared with those of the healthy control group by immunohistochemistry; and gradually upward tendency of TRIM21 expression in T cells was found among PBMCs, lymph nodes, and OLP lesions; and (4) TRIM21 overexpression significantly enhanced proliferation and interleukin-6 (IL-6) secretion of T cells. Conclusions Significantly high expression of TRIM21 in OLP lesions may be of great significance in the OLP immunopathologic mechanism. It is more likely that overexpressed TRIM21 in OLP lesions is a primary pathogenic molecule.

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