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辅助性T细胞 (Th) 1 Th2在数量、功能上的失衡是支气管哮喘发病机制中的重要环节。Th2优势分化及其分泌的白介素 (IL) 4、5、13等细胞因子介导了气道炎症和气道高反应性。信号转导子和转录激活子 6 (STAT6 )在Th2分化中起关键作用 ,而且是Th2分化的特异性转录因子 ,可促进Th2增殖和产生IL 4、IL 13等Th2型细胞因子。STAT6基因敲除小鼠在致敏和变应原激发后无气道高反应性和气道炎症的表现。因此 ,STAT6在变应原诱导的气道炎症中起着至关重要的作用 ,而且有望成为治疗哮喘的有效靶分子。
The quantitative and functional imbalance of helper T cell (Th) 1 Th2 is an important link in the pathogenesis of bronchial asthma. Th2 predominant differentiation and secretion of interleukin (IL) 4,5,13 and other cytokines mediate airway inflammation and airway hyperresponsiveness. Signal transducer and activator of transcription 6 (STAT6) play a key role in Th2 differentiation and are Th2-specific transcription factors that promote Th2 proliferation and produce Th2-type cytokines such as IL4 and IL13. STAT6 knockout mice showed no airway hyperresponsiveness and airway inflammation following sensitization and allergen challenge. Therefore, STAT6 plays a crucial role in allergen-induced airway inflammation and is expected to be an effective target for the treatment of asthma.