Hanada Toshitkatsu, Yoshimura Akihiko
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Cytokine Growth Factor Rev. 2002 Aug-Oct;13(4-5):413-21. doi: 10.1016/s1359-6101(02)00026-6.
Inflammation progresses by the action of pro-inflammatory cytokines, including interleukin-1 (IL-1), the tumor necrosis factor (TNF), gamma-interferon (IFNgamma), IL-12, IL-18, and the granulocyte-macrophage colony-stimulating factor, and is resolved by anti-inflammatory cytokines such as IL-4, IL-10, IL-13, IFNalpha, and the transforming growth factor (TGF)beta. The intracellular signal transduction pathways of these cytokines have been studied extensively, and these pathways ultimately activate transcription factors, such as NF-kappaB, Smad, and STATs. Recently, the negative-feedback regulation of these pathways has been identified. In this review, we provide examples of the relationship between cytokine signal transduction, negative-signal regulation, and inflammatory disease models. Furthermore, we illustrate several approaches for treating inflammatory diseases by modulating extracellular and intracellular signaling pathways.
炎症通过促炎细胞因子的作用而进展，这些促炎细胞因子包括白细胞介素-1（IL-1）、肿瘤坏死因子（TNF）、γ-干扰素（IFNγ）、IL-12、IL-18和粒细胞-巨噬细胞集落刺激因子，而炎症通过抗炎细胞因子如IL-4、IL-10、IL-13、IFNα和转化生长因子（TGF）β得以消退。这些细胞因子的细胞内信号转导途径已得到广泛研究，并且这些途径最终激活转录因子，如核因子κB（NF-κB）、Smad和信号转导子和转录激活子（STATs）。最近，已确定了这些途径的负反馈调节。在本综述中，我们提供细胞因子信号转导、负信号调节和炎症疾病模型之间关系的实例。此外，我们阐述了通过调节细胞外和细胞内信号通路来治疗炎症性疾病的几种方法。
