免疫组织化学
结缔组织
CD3型
间质细胞
川地69
牙周炎
病理
医学
慢性牙周炎
表型
生物
T细胞
免疫学
抗原
免疫系统
CD8型
白细胞介素2受体
内科学
基因
生物化学
作者
Federico Deli,Federica Romano,Giacomo Gualini,Giulia Maria Mariani,Irene Sala,Francesca Veneziano,Luca Bertero,Paola Cassoni,Mario Aimetti
摘要
Abstract Background/objectives Tissue‐resident memory T cells (Trm) represent a new subset of long‐lived memory T cells that remain in barrier tissues after previous bacterial or viral infection to support early/immediate defense mechanisms, providing site‐specific protection from pathogen challenge. As data on Trm cells in human gingiva are just emerging, the aim of the present study was to explore their presence and distribution in epithelial and connective periodontal tissues in relation to microbial exposure and periodontal damage. Material and methods Periodontitis tissue specimens were collected from 20 generalized chronic periodontitis patients at the time of osseous resective surgery. As a control, 18 healthy tissue specimens were harvested each from both the primary flap and the palatal graft in 18 periodontally healthy patients during mucogingival surgeries. As CD69 and CD103 are phenotypic markers associated with tissue residence, intraepithelial and stromal CD103+ and CD69+ cells per high‐power field were counted in areas with highest expression. Double immunohistochemistry for CD3 and CD69 was performed to identify T cells. Results CD69 +and CD103+ cells showed a lymphocytic morphology, and double CD69 and CD3 staining confirmed the T cell phenotype of these cells. CD103 and CD69 expression was significantly enhanced in epithelial and connective tissues from patients with periodontitis compared with healthy controls ( P < .001). Significant positive correlation between PD and both CD103 and CD69 epithelial expression was observed in tissue specimens from periodontitis patients ( P < .001). Conclusion Within the limits of the present study, these results indicate that Trm cells are higher in periodontitis lesions. They could orchestrate the host response to microbial challenge, leading to a faster reactivation of periodontal disease.
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