Kuga Taiga, Chiba Asako, Murayama Goh, Miyake Sachiko
Department of Immunology, Juntendo University Faculty of Medicine, Bunkyo-ku, Tokyo, Japan.
Department of Internal Medicine and Rheumatology, Juntendo University Faculty of Medicine, Bunkyo-ku, Tokyo, Japan.
Front Immunol. 2025 Jul 17;16:1562221. doi: 10.3389/fimmu.2025.1562221. eCollection 2025.
Type I interferons (IFNs) play crucial roles in the pathogenesis of systemic lupus erythematosus (SLE). Plasmacytoid dendritic cells (pDCs) stimulated by Toll-like receptor (TLR) pathways have been thought to be the major producers of IFNα in patients with SLE. However, the responsiveness of pDCs from SLE patients to stimuli that produce IFNα differs depending on the type of TLR pathway involved. In addition to pDCs, monocytes from SLE patients were found to produce IFNα when responding to the cGAS-STING pathway. Here, we outline the major pathways that induce IFNα production by myeloid cells in SLE, and the possible mechanisms by which IFNα overproduction occurs by these cells. Finally, we discuss the current and future therapeutic strategies to regulate IFNα production in patients with SLE.
I型干扰素（IFN）在系统性红斑狼疮（SLE）的发病机制中起关键作用。由Toll样受体（TLR）途径刺激的浆细胞样树突状细胞（pDC）被认为是SLE患者中IFNα的主要产生者。然而，SLE患者的pDC对产生IFNα的刺激的反应性因所涉及的TLR途径类型而异。除了pDC，还发现SLE患者的单核细胞在对cGAS-STING途径作出反应时会产生IFNα。在这里，我们概述了SLE中髓样细胞诱导IFNα产生的主要途径，以及这些细胞发生IFNα过量产生的可能机制。最后，我们讨论了调节SLE患者IFNα产生的当前和未来治疗策略。
