論文種別	原著(症例報告除く)
言語種別	英語
査読の有無	その他(不明)
表題	Dysbiosis of the gut microbiome may contribute to the pathogenesis of oral lichen planus through Treg dysregulation.
掲載誌名	正式名：Mucosal immunology 略　 称：Mucosal Immunol ISSNコード：19353456/19330219
掲載区分	国外
巻・号・頁	18(5),pp.1013-1026
著者・共著者	Shiho Yokomizo, Naoki Kaneko, Hu Chen, Lijing Yan, Shoji Tsuji, Shohei Akagawa, Junsei Sameshima, Tomoki Sueyoshi, Haruki Nagano, Yuka Miyahara, Yasuhisa Kamikaseda, Hajime Kido, Yoshikazu Hayashi, Masaki Yamauchi, Tamotsu Kiyoshima, Yuichi Goto, Yukiko Ohyama, Kazunari Kaneko, Masafumi Moriyama, Shintaro Kawano
発行年月	2025/10
概要	Oral lichen planus (OLP) is a chronic inflammatory disorder with autoimmune features and malignant transformation risk, lacking a definitive treatment, with CD4+ T cells being pivotal in its pathogenesis. Dysbiosis, an imbalance in the microbiome, is linked to various autoimmune and inflammatory diseases, where CD4+ T cells play a significant role. Given these insights, the development of OLP might be influenced by dysbiosis. This study investigates the association between dysbiosis and CD4+ T cells in OLP. We collected stool and saliva samples from OLP patients, conducting 16S rRNA gene analysis and mass spectrometry, and assessed CD4+ T cell characteristics in lesions through multiplex immunofluorescence and single-cell RNA sequencing. Peripheral blood samples were subjected to flow cytometry and cell culture assays. Results showed extensive gut dysbiosis in OLP patients, notably a reduction in short-chain fatty acid (SCFA)-producing bacteria essential for regulatory T cell (Treg) differentiation. While various CD4+ T cell subsets, including Tregs, were present in tissues, these Tregs as unresponsive to specific antigens, showing reduced immunosuppressive molecule expression. The decline in SCFA-producing bacteria correlated with fewer activated Tregs in tissues and blood. These findings suggest that gut dysbiosis may contribute to OLP by impairing Treg regulation, influencing disease pathogenesis.
DOI	10.1016/j.mucimm.2025.05.009
PMID	40499683