Case Report: Response of cutaneous lupus lesions in SLE to interferon receptor blockade parallels reduction of interferon score in blood

Claudia Günther; Christine Wolf; Louisa Fennen; Sarah Rösing; Stefan Beissert; Martin Aringer; Min Ae Lee-Kirsch

doi:10.3389/fimmu.2023.1253279

Case Report: Response of cutaneous lupus lesions in SLE to interferon receptor blockade parallels reduction of interferon score in blood

Front Immunol. 2023 Sep 21:14:1253279. doi: 10.3389/fimmu.2023.1253279. eCollection 2023.

Authors

Claudia Günther¹, Christine Wolf², Louisa Fennen¹, Sarah Rösing¹, Stefan Beissert¹, Martin Aringer³, Min Ae Lee-Kirsch²

Affiliations

¹ Department of Dermatology, University Hospital, Medizinische Fakultät Carl Gustav Carus, TU Dresden, Dresden, Germany.
² Department of Pediatrics, University Hospital, Medizinische Fakultät Carl Gustav Carus, TU Dresden, Dresden, Germany.
³ Division of Rheumatology, Department of Medicine III, University Medical Center Hospital TU Dresden, Dresden, Germany.

Abstract

Cutaneous lupus erythematosus (CLE), the main manifestation of systemic lupus erythematosus (SLE), is driven by type I interferons (IFNs) and often only partially responds to conventional therapies. Treatment of seven SLE patients with the monoclonal antibody anifrolumab induced fast and sustained remission of previously refractory CLE lesions, beginning within the first weeks of treatment. Decline in CLASI-A score was paralleled by a reduction in IFN score determined by mRNA expression of seven IFN-stimulated genes (ISGs) in blood. These data suggest that a subset of ISGs could be a valuable biomarker in CLE.

Keywords: CLASI; IFN score; anifrolumab; cutaneous lupus; interferon.

Publication types

Case Reports
Research Support, Non-U.S. Gov't

MeSH terms

Antibodies, Monoclonal / therapeutic use
Humans
Interferon Type I*
Lupus Erythematosus, Cutaneous* / diagnosis
Lupus Erythematosus, Cutaneous* / drug therapy
Lupus Erythematosus, Systemic* / diagnosis
Lupus Erythematosus, Systemic* / drug therapy
Receptors, Interferon

Substances

Receptors, Interferon
Interferon Type I
Antibodies, Monoclonal

Grants and funding

The project was funded by grants from the German Research Foundation (Deutsche 160 Forschungsgemeinschaft) CRC237, 369799452 to CG, CRC237 369799452/A06 to CW CRC237, CRC237 369799452/B21 and CRC237 369799452/A11 to M.L.-K., and the Federal Ministry of Education and Research (BMBF GAIN 01GM2206C to M.L.-K.). CG received support from GSK, AstraZeneca, and Boehringer. The funders were not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication.