Lai Yuping, Dong Chen
Shanghai Key Laboratory of Regulatory Biology, School of Life Science, East China Normal University, No.500 Minhang Dongchuan Road, Shanghai 200241, China.
Institute for Immunology, Tsinghua University, Medical Research Building D330, No.30 Haidian Shuangqing Road, Beijing 100084, China
Int Immunol. 2016 Apr;28(4):181-8. doi: 10.1093/intimm/dxv063. Epub 2015 Nov 6.
Inflammatory cytokines are key regulators of immune responses. Persistent and excessive production of inflammatory cytokines underscores the development of autoimmune diseases. Therefore, neutralizing inflammatory cytokines or antagonizing their receptor function is considered as a useful therapeutic strategy to treat autoimmune diseases. To achieve the success of such a strategy, understanding of the complex actions of these cytokines and cytokine networks is required. In this review we focus on four inflammatory cytokines--tumor necrosis factor α (TNFα), interleukin-6 (IL-6), IL-23 and IL-17--and dissect how the dysregulation of these cytokines regulates autoimmune diseases. On the basis of pre-clinical and clinical data, we specifically discuss the therapeutic rationale for targeting these cytokines and describe the potential adverse effects.
炎性细胞因子是免疫反应的关键调节因子。炎性细胞因子的持续过量产生是自身免疫性疾病发展的重要原因。因此，中和炎性细胞因子或拮抗其受体功能被认为是治疗自身免疫性疾病的有效策略。为了实现这一策略的成功，需要了解这些细胞因子和细胞因子网络的复杂作用。在本综述中，我们聚焦于四种炎性细胞因子——肿瘤坏死因子α（TNFα）、白细胞介素-6（IL-6）、IL-23和IL-17——并剖析这些细胞因子的失调如何调节自身免疫性疾病。基于临床前和临床数据，我们特别讨论了针对这些细胞因子的治疗原理，并描述了潜在的不良反应。
