Systemic lupus erythematosus (SLE) is a highly prevalent autoimmune disease characterized by the malfunction of the immune system and the persistent presence of an inflammatory environment. Multiple organs can be affected during SLE, leading to heterogeneous manifestations, which eventually result in the death of patients. Due to the lack of understanding regarding the pathogenesis of SLE, the currently available treatments remain suboptimal. Sphingosine-1-phosphate (S1P) is a central bioactive lipid of sphingolipid metabolism, which serves a pivotal role in regulating numerous physiological and pathological processes. As a well-recognized regulator of lymphocyte trafficking, S1P has been shown to be closely associated with autoimmune diseases, including SLE. Importantly, S1P levels have been found to be elevated in patients with SLE. In murine models of lupus, the increased levels of S1P also contribute to disease activity and organ impairment. Moreover, data from several studies also support the hypothesis that S1P receptors and its producer—sphingosine kinases (SPHK) may serve as the potential targets for the treatment of SLE and its co-morbidities. Given the significant success that intervening with S1P signaling has achieved in treating multiple sclerosis, further exploration of its role in SLE is necessary. Therefore, the aim of the present review is to summarize the recent advances in understanding the potential mechanism by which S1P influences SLE, with a primary focus on its role in immune regulation and inflammatory responses.

系统性红斑狼疮 (SLE) 是一种高度流行的自身免疫性疾病，其特征是免疫系统功能障碍和炎症环境持续存在。 SLE 期间多个器官可能受到影响，导致异质性表现，最终导致患者死亡。由于缺乏对 SLE 发病机制的了解，目前可用的治疗方法仍然不够理想。 1-磷酸鞘氨醇 (S1P) 是鞘脂代谢的核心生物活性脂质，在调节许多生理和病理过程中发挥着关键作用。作为公认的淋巴细胞运输调节因子，S1P 已被证明与包括 SLE 在内的自身免疫性疾病密切相关。重要的是，已发现 SLE 患者的 S1P 水平升高。在狼疮小鼠模型中，S1P 水平升高也会导致疾病活动和器官损伤。此外，多项研究的数据也支持这样的假设：S1P 受体及其产生者——鞘氨醇激酶 (SPHK) 可能作为治疗 SLE 及其并发症的潜在靶点。鉴于干预 S1P 信号传导在治疗多发性硬化症方面取得了巨大成功，有必要进一步探索其在 SLE 中的作用。因此，本综述的目的是总结 S1P 影响 SLE 潜在机制的最新进展，重点关注其在免疫调节和炎症反应中的作用。