Ryu Gwanghui, Bae Jun-Sang, Yoo Shin Hyuk, Kim Eun Hee, Mo Ji-Hun
Department of Otorhinolaryngology-Head and Neck Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 06351, Republic of Korea.
Department of Otorhinolaryngology, Dankook University College of Medicine, 201 Manghyang-Ro, Dongnam-Gu, Cheonan, 31116, Republic of Korea.
Inflammation. 2025 Jan 4. doi: 10.1007/s10753-024-02227-8.
During nasal polyp (NP) development, activated T cells differentiate into T helper (Th) 1, Th2, and Th17 cells. Additionally, regulatory T cells (Tregs) that have an immune suppressive function are involved in the pathophysiology of chronic rhinosinusitis (CRS) with NP (CRSwNP). Tregs can act as effector cells that produce inflammatory cytokines, such as interleukin (IL)-17A. We sought to identify the cellular expression of IL-17A and Treg markers in sinonasal tissue from CRSwNP patients and to investigate whether Tregs are involved in IL-17A secretion. The uncinate process (UP) and NP tissues were harvested from patients with CRSwNP, CRS without NP (CRSsNP), and normal controls. Expression of IL-17A and Foxp3 in each group was observed with immunohistochemistry and immunofluorescence. Expression of IL-17A in Treg was evaluated by flow cytometry of single cells isolated from sinonasal tissues. UP tissue from controls (n = 17), UP from CRSsNP (n = 24), and UP (n = 19) and NP (n = 29) from CRSwNP were obtained. The percentage of Foxp3 cells was higher in CRS tissues compared with normal controls. IL-17A cells were most increased in NP tissues from CRSwNP patients. Expression of IL-17A in some Foxp3 cells was observed in double immunofluorescence. Foxp3 cells, IL-17A cells, and Foxp3IL-17A cells were increased in the UP and NP tissues from CRSwNP patients. CD45RAFoxp3 cells were increased in CRSwNP, and IL-17A cells were observed most frequently in CD4CD45RAFoxp3 cells from NP tissues. These findings show that CD4CD45RAFoxp3 Tregs are involved in NP pathogenesis by producing IL-17A.
在鼻息肉（NP）发生过程中，活化的T细胞分化为辅助性T（Th）1、Th2和Th17细胞。此外，具有免疫抑制功能的调节性T细胞（Tregs）参与了伴NP的慢性鼻-鼻窦炎（CRS）（CRSwNP）的病理生理过程。Tregs可作为产生炎性细胞因子（如白细胞介素（IL）-17A）的效应细胞。我们试图确定CRSwNP患者鼻窦组织中IL-17A和Treg标志物的细胞表达情况，并研究Tregs是否参与IL-17A的分泌。从CRSwNP患者、无NP的CRS（CRSsNP）患者及正常对照者获取钩突（UP）和NP组织。采用免疫组织化学和免疫荧光法观察各组中IL-17A和Foxp3的表达。通过对从鼻窦组织分离的单细胞进行流式细胞术评估Treg中IL-17A的表达。获取了对照组的UP组织（n = 17）、CRSsNP的UP组织（n = 24）以及CRSwNP的UP组织（n = 19）和NP组织（n = 29）。与正常对照相比，CRS组织中Foxp3细胞的百分比更高。CRSwNP患者NP组织中IL-17A细胞增加最为明显。在双重免疫荧光中观察到部分Foxp3细胞中有IL-17A表达。CRSwNP患者的UP和NP组织中Foxp3细胞、IL-17A细胞及Foxp3IL-17A细胞均增加。CRSwNP中CD45RAFoxp3细胞增加，且在NP组织的CD4CD45RAFoxp3细胞中最常观察到IL-17A细胞。这些发现表明，CD4CD45RAFoxp3 Tregs通过产生IL-17A参与NP的发病机制。
