Musculoskeletal Research Group, Institute of Cellular Medicine, Faculty of Medicine, Newcastle University, Newcastle upon Tyne, UK.
Biofactors. 2013 Nov-Dec;39(6):593-6. doi: 10.1002/biof.1117. Epub 2013 Jul 25.
Chronic inflammation can lead to altered extracellular matrix deposition and ultimately fibrosis. Interleukin-13 (IL-13) is a cytokine that was found to promote IgE class switching and inhibit proinflammatory cytokines. However, it is now recognized as an important mediator in allergy and most importantly fibrosis. Indeed, animal studies with genetically deleted mice have demonstrated its critical role in fibrosis and although it shares over lapping functions with IL-4 it is the dominant cytokine in fibrosis. Systemic sclerosis is an autoimmune disease in which there is chronic inflammation and fibrosis. The disease is associated with a Th2 polarization and IL-13 levels are elevated both in the blood and in the skin of patients. This review will examine the role of IL-13 in driving fibrosis with a particular emphasis on systemic sclerosis as a prototypical fibrotic disease. It will highlight recent research into the role of IL-13 and how this cytokine may be targeted in systemic sclerosis.
慢性炎症可导致细胞外基质沉积改变，最终导致纤维化。白细胞介素 13（IL-13）是一种细胞因子，可促进 IgE 类转换并抑制促炎细胞因子。然而，它现在被认为是过敏反应的重要介质，尤其是纤维化。实际上，用基因缺失小鼠进行的动物研究表明，它在纤维化中具有关键作用，尽管它与 IL-4 具有重叠的功能，但它是纤维化中的主要细胞因子。系统性硬化症是一种自身免疫性疾病，其特征为慢性炎症和纤维化。该疾病与 Th2 极化有关，患者的血液和皮肤中均升高白细胞介素 13 水平。这篇综述将检查白细胞介素 13 在驱动纤维化中的作用，特别强调系统性硬化症作为典型的纤维化疾病。它将重点介绍白细胞介素 13 作用的最新研究以及该细胞因子如何在系统性硬化症中被靶向。
