1 Department of Clinical Immunology at Sun Yat-sen University Third Hospital, Guangzhou, China.
2 Division of Rheumatology, Penn State College of Medicine and Milton S. Hershey Medical Center, Hershey, PA, USA.
Lupus. 2019 Apr;28(5):575-582. doi: 10.1177/0961203319829818. Epub 2019 Apr 5.
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease with immune system disorder mediated through complex autoimmune pathways that involve immune cells, nonimmune cells, cytokines, chemokines, as well as costimulatory molecules. Costimulatory signals play a critical role in initiating, maintaining and regulating immune reactions, and these include ligands and receptors and their interactions involving multiple types of signal information. Dysfunction of costimulatory factors results in complicated abnormal immune responses, with biological effects and eventually, clinical autoimmune diseases. Here we outline what is known about various roles that costimulatory families including the B7 family and tumor necrosis factor super family play in SLE. The aim of this review is to understand the possible association of costimulation with autoimmune diseases, especially SLE, and to explore possible therapeutic target(s) of costimulatory molecules and pathways that might be used to develop therapeutic approaches for patients with these conditions.
系统性红斑狼疮（SLE）是一种慢性炎症性疾病，其免疫系统紊乱是通过复杂的自身免疫途径介导的，涉及免疫细胞、非免疫细胞、细胞因子、趋化因子以及共刺激分子。共刺激信号在启动、维持和调节免疫反应中起着关键作用，这些信号包括配体和受体及其涉及多种类型信号信息的相互作用。共刺激因子功能障碍导致复杂的异常免疫反应，产生生物学效应，最终导致临床自身免疫性疾病。本文概述了共刺激家族（包括 B7 家族和肿瘤坏死因子超家族）在 SLE 中的各种作用。本文的目的是了解共刺激与自身免疫性疾病（特别是 SLE）的可能关联，并探讨共刺激分子和途径的可能治疗靶点，这些靶点可能用于为这些疾病患者开发治疗方法。
