Expression of programmed death 1 ligand 1 on periodontal tissue cells as a possible protective feedback mechanism against periodontal tissue destruction

牙周组织细胞上程序性死亡配体1的表达可能是一种抵抗牙周组织破坏的保护性反馈机制。

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作者:Jiehua Zhang ,Chieh-Mei Wang ,Ping Zhang ,Xiaoqian Wang ,Jiao Chen ,Jun Yang ,Wanlu Lu ,Wenjie Zhou ,Wenwen Yuan ,Yun Feng

Abstract

Programmed death 1 ligand 1 (PD‑L1) is a negative co‑stimulatory molecule in immune responses. Previous reports have indicated that inflammatory cytokines can upregulate the expression of PD‑L1 in tumor cells, which in turn suppresses host immune responses. Periodontitis is characterized by persistent inflammation of the periodontium, which is initiated by infection with oral bacteria and results in damage to cells and the matrices of the periodontal connective tissues. In the present study, the expression and function of PD‑L1 in periodontal tissue destruction were examined. Periodontal ligament cells (PDLCs) were stimulated by inflammatory cytokines and periodontal pathogens. The expression and function of PD‑L1 on the surface of PDLCs was investigated using flow cytometry in vitro. Periodontal disease was induced by the injection of Porphyromonas gingivalis in mouse models. The expression levels of PD‑L1 in the periodontal tissues of the mice were analyzed using flow cytometry and immunohistochemistry. PD‑L1 was inducibly expressed on the PDLCs by the inflammatory cytokines and periodontal pathogens. The inflammation‑induced expression of PD‑L1 was shown to cause the apoptosis of activated T lymphocytes and improve the survival of PDLCs. Furthermore, in the mouse model of experimental periodontitis, the expression of PD‑L1 in severe cases of periodontitis was significantly lower, compared with that in mild cases. By contrast, no significant differences were observed between the healthy control and severe periodontitis groups. The results of the present study showed that the expression of PD‑L1 may inhibit the destruction of periodontal tissues, indicating the involvement of a possible protective feedback mechanism against periodontal infection.

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