STAT6 and lung inflammation.
STAT6 and lung inflammation.
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DOI：
10.4161/jkst.25301
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发表时间：
2013-10-01
期刊：
影响因子：
--
通讯作者：
Doherty TA
中科院分区：
文献类型：
--
作者：
Walford HH;Doherty TA
肺部炎症有许多病因，包括Th 2型免疫疾病，如哮喘和抗寄生虫反应。肺的炎性疾病涉及结构细胞（气道上皮、平滑肌和成纤维细胞）和免疫细胞（B和T细胞、巨噬细胞、树突状细胞和先天性淋巴细胞）之间的复杂相互作用。在动物模型中，信号转导子和转录激活子6（STAT 6）已被证实可调节肺炎症反应的许多病理特征，包括气道嗜酸性粒细胞增多、上皮粘液产生、平滑肌变化、Th 2细胞分化和B细胞IgE产生。发现STAT 6上游的细胞因子IL-4和IL-13在人类哮喘中升高，并且正在进行临床试验以治疗靶向IL-4/IL-13/STAT 6通路。此外，最近的研究表明，STAT 6也可能调节肺抗病毒反应，并有助于肺纤维化。本文将重点介绍STAT 6在肺部疾病中的作用以及STAT 6控制免疫和结构肺细胞功能的机制。
Lung inflammation has many etiologies, including diseases of Th2-type immunity, such as asthma and anti-parasitic responses. Inflammatory diseases of the lung involve complex interactions among structural cells (airway epithelium, smooth muscle, and fibroblasts) and immune cells (B and T cells, macrophages, dendritic cells, and innate lymphoid cells). Signal transducer and activator of transcription 6 (STAT6) has been demonstrated to regulate many pathologic features of lung inflammatory responses in animal models including airway eosinophilia, epithelial mucus production, smooth muscle changes, Th2 cell differentiation, and IgE production from B cells. Cytokines IL-4 and IL-13 that are upstream of STAT6 are found elevated in human asthma and clinical trials are underway to therapeutically target the IL-4/IL-13/STAT6 pathway. Additionally, recent work suggests that STAT6 may also regulate lung anti-viral responses and contribute to pulmonary fibrosis. This review will focus on the role of STAT6 in lung diseases and mechanisms by which STAT6 controls immune and structural lung cell function.