Systemic lupus erythematosus (SLE) is a potentially fatal chronic autoimmune disease which is underlain by complex dysfunction of the innate and adaptive immune systems. Although a series of well-defined genetic and environmental factors have been implicated in disease etiology, neither the development nor the persistence of SLE is well understood. Given that several disease susceptibility genes and environmental factors interact and influence inflammatory lineage specification through metabolism, the field of immunometabolism has become a forefront of cutting edge research. Along these lines, metabolic checkpoints of pathogenesis have been identified as targets of effective therapeutic interventions in mouse models and validated in clinical trials. Ongoing studies focus on mitochondrial oxidative stress, activation of the mechanistic target of rapamycin, calcium signaling, glucose utilization, tryptophan degradation, and metabolic cross-talk between gut microbiota and the host immune system.

中文翻译：

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系统性红斑狼疮的免疫代谢

系统性红斑狼疮 (SLE) 是一种潜在致命的慢性自身免疫性疾病，其病因是先天性和适应性免疫系统的复杂功能障碍。尽管一系列明确的遗传和环境因素与疾病病因有关，但系统性红斑狼疮的发展和持续情况尚不清楚。鉴于多种疾病易感基因和环境因素通过代谢相互作用并影响炎症谱系规范，免疫代谢领域已成为前沿研究的前沿。沿着这些思路，发病机制的代谢检查点已被确定为小鼠模型中有效治疗干预的目标，并在临床试验中得到验证。正在进行的研究重点是线粒体氧化应激、雷帕霉素机制靶标的激活、钙信号传导、葡萄糖利用、色氨酸降解以及肠道微生物群与宿主免疫系统之间的代谢串扰。