REVIEW article

Front. Immunol.

Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1562221

This article is part of the Research TopicCommunity Series in The Role of Monocytes/Macrophages in Autoimmunity and Autoinflammation: Volume IIView all 6 articles

Myeloid cells as IFNα producers in systemic lupus erythematosus

Provisionally accepted
  • 1Department of Immunology, Faculty of Medicine, Juntendo University, Tokyo, Japan
  • 2Department of Internal Medicine and Rheumatology, Faculty of Medicine, Juntendo University, Tokyo, Japan

The final, formatted version of the article will be published soon.

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 to 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.

Keywords: SLE, pDc, monocyte, interferon, TLR, cGAS-STING, cellular senescence

Received: 17 Jan 2025; Accepted: 01 Jul 2025.

Copyright: © 2025 Kuga, Chiba, Murayama and Miyake. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Asako Chiba, Department of Immunology, Faculty of Medicine, Juntendo University, Tokyo, Japan
Sachiko Miyake, Department of Immunology, Faculty of Medicine, Juntendo University, Tokyo, Japan

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