A promising approach to targeting type 1 IFN in systemic lupus erythematosus
Yashaar Chaichian,1 Daniel J. Wallace,2 and Michael H. Weisman2
1Division of Immunology and Rheumatology, Stanford University, Palo Alto, California, USA.
2Division of Rheumatology, Cedars-Sinai Medical Center, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Address correspondence to: Yashaar Chaichian, 1000 Welch Rd., Suite 203, MC 5755, Division of Immunology and Rheumatology, Stanford University, Palo Alto, California 94304, USA. Phone: 650.725.8004; Email: ychaich@stanford.edu.
Find articles by Chaichian, Y. in: JCI | PubMed | Google Scholar
1Division of Immunology and Rheumatology, Stanford University, Palo Alto, California, USA.
2Division of Rheumatology, Cedars-Sinai Medical Center, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Address correspondence to: Yashaar Chaichian, 1000 Welch Rd., Suite 203, MC 5755, Division of Immunology and Rheumatology, Stanford University, Palo Alto, California 94304, USA. Phone: 650.725.8004; Email: ychaich@stanford.edu.
Find articles by Wallace, D. in: JCI | PubMed | Google Scholar
1Division of Immunology and Rheumatology, Stanford University, Palo Alto, California, USA.
2Division of Rheumatology, Cedars-Sinai Medical Center, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Address correspondence to: Yashaar Chaichian, 1000 Welch Rd., Suite 203, MC 5755, Division of Immunology and Rheumatology, Stanford University, Palo Alto, California 94304, USA. Phone: 650.725.8004; Email: ychaich@stanford.edu.
Find articles by Weisman, M. in: JCI | PubMed | Google Scholar
First published February 18, 2019 - More info
J Clin Invest. 2019;129(3):958–961. https://doi.org/10.1172/JCI127101.
Copyright © 2019, American Society for Clinical Investigation
Despite advances in understanding systemic lupus erythematosus (SLE) pathogenesis, most clinical trials of new targeted therapies have been met with disappointment. The type I IFN pathway is believed to play an important role in SLE, and the proposed involvement of this pathway helps explain the frustration behind the failure at targeting either IFN-α or the type 1 IFN receptor itself. In this issue of the JCI, Furie et al. report on an intriguing phase 1b study that demonstrates an approach for inhibiting this pathway in the skin using an mAB (BIIB059) that targets the blood DC antigen 2 (BDCA-2) receptor on plasmacytoid DCs (pDCs). BIIB059 decreased IFN expression and improved cutaneous lupus disease activity, with a favorable safety profile. Whether or not this strategy will be effective in managing SLE in other organs remains unanswered. However, these results suggest that closing the door on targeting the type 1 IFN pathway in SLE may be premature and highlight the emerging question of whether an organ-specific approach toward lupus trials and treatment should be the wave of the future.
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