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由TIM-3驱动的巨细胞极化与具有鼻息肉的复发性慢性鼻炎有关

Tao Jiang¹, Tao Yu¹, Lu Jiang¹

¹Department of Otolaryngology-Head and Neck Surgery, Changde Hospital, Xiangya School of Medicine, Central South University (The First People's Hospital of Changde City), Changde, China.

Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale

|September 30, 2024

概括

含有-3 (TIM-3) 的T细胞免疫球蛋白和粘素域的表达在具有鼻息肉的慢性鼻炎 (CRSwNP) 中升高,特别是在复发的情况下. TIM-3促进M2巨细胞的两极分化,这表明它在反抗性CRSwNP中的作用.

科学领域:

免疫学免疫学免疫学
耳鼻喉科耳鼻喉科耳鼻喉科
病理生理学病理生理学

背景情况:

带鼻息肉的慢性鼻炎 (CRSwNP) 是一种复杂的炎症状况.
重复性CRSwNP,特别是在修复手术后,提出了重大的临床挑战.
像TIM-3这样的特定免疫标记物在CRSwNP病变发生中的作用仍然不完全理解.

研究的目的:

在CRSwNP患者中评估T细胞免疫球蛋白和含有-3 (TIM-3) 的粘素域的表达.
调查TIM-3对CRSwNP.巨细胞极化的影响.
探索TIM-3作为反抗性CRSwNP的潜在生物标志物.

主要方法:

从健康对照 (HC),初级CRSwNP和复发性CRSwNP患者的血清和组织样本中量化了TIM-3表达.
宏细胞极化标志物 (CD163,CD206) 被评估并与TIM-3水平相关联.
在体外实验中,研究了TIM-3过度表达对巨细胞极化和细胞因子分泌 (TGF-β1,IL-10) 的影响.

主要成果:

与HC相比,CRSwNP患者的TIM-3水平显著更高,在复发病例中表达率升高.
组织免疫光检测证实CRSwNP中的TIM-3表达增加,与CD163和CD206.6正相关.
过度表达TIM-3诱导了M2巨细胞两极分化,并增加了TGF-β1和IL-10的分泌.

结论:

提升的TIM-3表达与CRSwNP有关,特别是在需要修复手术的患者中.
TIM-3可以作为一种新的生物标志物,用于识别和管理固的CRSwNP.
由TIM-3介导的M2巨细胞极化与复发性CRSwNP的病理生理学有关.

关键词:

在TIM-3中,TIM-3是TIM-3.慢性鼻炎与鼻多.巨细胞是一个巨细胞.复发性复发性复发性

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