IL-13和替代激活的巨噬细胞在纤维化中的作用

The role of IL-13 and alternative activated macrophages in fibrosis

纤维化是由于炎症导致器官实质细胞发生坏死,纤维结缔组织异常增多和过度沉积的病理过程.大量的研究表明,IL-13参与了纤维化的发生发展过程,其各种功能通过复杂受体系统来完成,包括IL-13受体a1（IL-13 Ra1）,IL-4受体（IL-4R）和IL-13受体a2（IL-13Ra2）.此外,IL-13和IL-4可激活巨噬细胞表型转变为替代激活的巨噬细胞,发挥促纤维化的作用,现概括介绍IL-13及其受体、替代激活的巨噬细胞在纤维化中的作用研究的新进展.

Fibrosis results from inflammation,which triggers necrosis of organ parenchymal cells and excessive deposits of fibrous connective tissue.Numerous studies have suggested that Interleukin 13 （IL-13）involves in the process of fibrosis.Its diverse fuctions are mediated by a complicated receptor system in IL-13 receptor a1 （IL-13Ra1）,IL-4 receptor a（IL-4R）,and IL-13 receptor a2（IL-13Ra2）.In addition,IL-13 and IL-4 induce alternative activation of macrophages to promote fibrosis.This review focuses on the roles of IL-13,its receptors,and macrophage in fibrosis alternative activation macrophages in fibrosis.