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已发表论文
溃疡性口腔黏膜疾病中角质形成细胞与 T 细胞的相互作用：上皮功能障碍的机制及治疗前景
Authors Hao Y , Yuan Y, Yu Y, Liu C, Wang Z, Li Y, Chen Q
Received 27 May 2025
Accepted for publication 30 September 2025
Published 16 October 2025 Volume 2025:18 Pages 14405—14421
DOI https://doi.org/10.2147/JIR.S543082
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Ning Quan
Yilong Hao,1,* Yao Yuan,2,* Yang Yu,1 Chuanxia Liu,1 Zhiyong Wang,1 Yining Li,1 Qianming Chen1
1Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, Hangzhou, Zhejiang, 310000, People’s Republic of China; 2State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yining Li, Email liyn@zju.edu.cn Qianming Chen, Email qmchen@zju.edu.cn
Abstract: Erosive and ulcerative oral mucosal diseases (OMDs) are characterized by persistent inflammation, epithelial barrier disruption, and impaired tissue repair, including oral lichen planus (OLP), discoid lupus erythematosus (DLE), pemphigus vulgaris (PV), mucous membrane pemphigoid (MMP), and recurrent aphthous ulcers (RAU). Aberrant activation of T cells induces cytotoxic and cytokine-mediated injury to the oral mucosa, impairing epithelial stem cell (EpSC) function, damaging the basement membrane, and compromising epithelial regeneration, which eventually results in sustained barrier failure. Under physiological conditions, EpSCs maintain mucosal resilience through continuous self-renewal and rapid turnover. In ulcerative OMDs, however, T cells drive inflammatory signals disrupt these processes. To systematically understand these mechanisms, this review summarizes current evidence on disease specific T cell subsets, cytokine networks, and keratinocyte responses that drive oral epithelial dysfunction. It also highlights emerging therapeutic strategies aimed at restoring epithelial homeostasis by targeting T cell and keratinocyte interactions.
Keywords: epithelial stemness, keratinocytes, oral mucosal diseases, mucosa immunity, T cell
1Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, Hangzhou, Zhejiang, 310000, People’s Republic of China; 2State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yining Li, Email liyn@zju.edu.cn Qianming Chen, Email qmchen@zju.edu.cn
Abstract: Erosive and ulcerative oral mucosal diseases (OMDs) are characterized by persistent inflammation, epithelial barrier disruption, and impaired tissue repair, including oral lichen planus (OLP), discoid lupus erythematosus (DLE), pemphigus vulgaris (PV), mucous membrane pemphigoid (MMP), and recurrent aphthous ulcers (RAU). Aberrant activation of T cells induces cytotoxic and cytokine-mediated injury to the oral mucosa, impairing epithelial stem cell (EpSC) function, damaging the basement membrane, and compromising epithelial regeneration, which eventually results in sustained barrier failure. Under physiological conditions, EpSCs maintain mucosal resilience through continuous self-renewal and rapid turnover. In ulcerative OMDs, however, T cells drive inflammatory signals disrupt these processes. To systematically understand these mechanisms, this review summarizes current evidence on disease specific T cell subsets, cytokine networks, and keratinocyte responses that drive oral epithelial dysfunction. It also highlights emerging therapeutic strategies aimed at restoring epithelial homeostasis by targeting T cell and keratinocyte interactions.
Keywords: epithelial stemness, keratinocytes, oral mucosal diseases, mucosa immunity, T cell