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JNJ-473 Could be a Novel Treatment for SLE

June 9 2016 11:28 AM ET via RheumReports RheumReports

Plasmocytoid Dendritic Cells (pDC) are potent producers of interferon (IFN) in SLE patients who express high CD123. It is known that JNJ-473 binds to CD123 (IL-3Rα).

A study presented by Katherine Monaghan from Australia aimed to determine the in vitro effects of JNJ-473 on SLE and its ability to deplete pDC. Forty SLE patients with a wide range of disease activity were evaluated and compared to age- and sex-matched controls (healthy donor blood samples).

The results suggest that in SLE patients, CD123 is expressed on different cell subsets. SLE patients had reduced pDC counts and highly expressed CD123. 

More importantly, depletion of pDC was achieved with JNJ-473 via NK antibody-dependent cell-mediated cytotoxicity (ADCC). JNJ-473 was able to inhibit the IFN gene signature induced by the SLE immune complex.

The bottom line is that JNJ-473 could be a novel treatment strategy for SLE by inhibiting the IFN gene signature. Further studies are needed to determine the role of JNJ-473 in vivo in SLE patients.

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About the Author

Dr. Zahi Touma
Dr. Zahi Touma

Dr. Touma is a clinical epidemiologist and an Assistant Professor of Medicine in the Division of Rheumatology at the University of Toronto, and Staff Physician and Clinician Scientist in the Division of Rheumatology, Toronto Western Hospital and Mount Sinai Hospital. In 2012 he completed his PhD in Clinical Epidemiology and subsequently completed one year of post-doctoral work in Measurement in Clinical Research.

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