T-cell senescence and immunosenescence in chronic oral mucosal inflammatory diseases: mechanisms and therapeutic implications.
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..
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.
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.
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.
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.
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.
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.
Authors
Qiu Qiu, Luo Luo, Pu Pu, Luo Luo, Jiang Jiang, Nasser Nasser, Liu Liu, Yalikun Yalikun
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