Journal of oral microbiology · 2026
T-cell senescence and immunosenescence in chronic oral mucosal inflammatory diseases: mechanisms and therapeutic implications.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Qiu Huaijue, Luo Yilin, Pu Lei, Luo Xue, Jiang Xiliang, Nasser Moussa Ide, Liu Chi, Yalikun Kaidiliya
Аннотация
BACKGROUND: The oral mucosa is a dynamic barrier. T‑cell dysregulation contributes to chronic oral mucosal inflammatory diseases, but the role of age‑related immune remodeling remains unclear..
METHOD: We performed a narrative review of PubMed/Medline (1972-2026) on T‑cell subsets, immunosenescence, exhaustion, and inflammation in oral lichen planus (OLP), Behçet's disease (BD), and recurrent aphthous stomatitis (RAS). After screening, we synthesized 121 publications.
RESULTS: Disease‑specific patterns emerged. In OLP, activated CD8⁺ and tissue‑resident memory T cells associate with basal keratinocyte injury, while senescent mesenchymal cells may amplify inflammation via SASP. In BD, Th1/Th17 polarization, reduced regulatory control, and neutrophil activation drive systemic and mucosal inflammation. In RAS, Th1‑skewed and CD8⁺ responses correlate with epithelial damage. Direct causal evidence for senescent or exhausted T cells is limited, especially for BD and RAS.
CONCLUSION: T‑cell senescence may modulate disease course, but its effects are context‑dependent rather than universal drivers. The strongest support exists for senescence‑associated stromal signaling in OLP; evidence in BD and RAS is mainly associative. Therapeutic strategies targeting senescence remain hypothesis‑generating and largely preclinical.
METHOD: We performed a narrative review of PubMed/Medline (1972-2026) on T‑cell subsets, immunosenescence, exhaustion, and inflammation in oral lichen planus (OLP), Behçet's disease (BD), and recurrent aphthous stomatitis (RAS). After screening, we synthesized 121 publications.
RESULTS: Disease‑specific patterns emerged. In OLP, activated CD8⁺ and tissue‑resident memory T cells associate with basal keratinocyte injury, while senescent mesenchymal cells may amplify inflammation via SASP. In BD, Th1/Th17 polarization, reduced regulatory control, and neutrophil activation drive systemic and mucosal inflammation. In RAS, Th1‑skewed and CD8⁺ responses correlate with epithelial damage. Direct causal evidence for senescent or exhausted T cells is limited, especially for BD and RAS.
CONCLUSION: T‑cell senescence may modulate disease course, but its effects are context‑dependent rather than universal drivers. The strongest support exists for senescence‑associated stromal signaling in OLP; evidence in BD and RAS is mainly associative. Therapeutic strategies targeting senescence remain hypothesis‑generating and largely preclinical.