IRF5公司
共域化
牙周炎
免疫组织化学
病理
川地68
根尖周炎
医学
肿瘤坏死因子α
巨噬细胞
慢性牙周炎
免疫系统
生物
免疫学
干扰素调节因子
内科学
先天免疫系统
分子生物学
体外
生物化学
作者
Jingjing Yu,Huan Zhao,Guojing Liu,Lingxin Zhu,Bin Peng
标识
DOI:10.1016/j.joen.2022.03.003
摘要
Interferon regulatory factor 5 (IRF5) is critical for the regulation of immune and inflammatory responses in health and diseases. However, the presence of IRF5 in human apical periodontitis remains unknown. This study aimed to explore the expression and colocalization of IRF5 with tumor necrosis factor receptor-associated factor 6 (TRAF6) and AKT2 in human apical periodontitis.A total of 39 human periapical tissues, including healthy gingival tissues (n = 12), periapical granulomas (PGs, n = 13), and radicular cysts (RCs, n = 14), were used in this study. The inflammatory infiltrates of lesions were evaluated by hematoxylin-eosin staining. The expression of IRF5 was detected by immunohistochemistry. Double immunofluorescence assessment was performed to colocalize IRF5 with CD68, TRAF6, and AKT2, respectively. Data were analyzed using the Kruskal-Wallis test.Immunohistochemistry revealed significantly higher expressions of IRF5 in PGs and RCs than the healthy control group. IRF5-CD68 double-positive cells were more predominant in RCs and PGs than the healthy control group. Significant differences of the IRF5-TRAF6 and IRF5-AKT2 double-positive cells were detected in periapical lesions compared with the healthy control tissues.IRF5 was highly expressed in macrophages of human periapical tissues and was colocalized with TRAF6 or AKT2 in human periapical tissues. These findings may provide new clues for understanding the pathogenesis of periapical diseases.
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