Approximately 1.5 million individuals in the United States suffer from systemic lupus erythematosus (SLE). Standard of care treatments for SLE include oral steroids, mycophenolic acid, hydroxychloroquine, B cell targeting therapies (rituximab), and type-1 interferon targeting therapies (anifrolumab, sifalimumab). All of these therapies relieve the symptoms but do not treat the root cause of the disease. Genetic analysis of SLE has implicated ~100 genetic variants associated with the disease across ethnicities suggesting a complex etiology. Mapping the cell types and cell states underlying the etiology and pathogenesis of the disease remains incomplete and annotating the molecular function of disease-associated variants has been challenging.
Investigators at the University of California, San Francisco used high throughput singe-cell RNAseq to identify three cell states, each displaying unique biomarkers that are more highly abundant in SLE patients compared to healthy individuals. These cell types can serve as novel therapeutic targets for therapies such as small molecules, antibodies, recombinant T-cell, or chimeric antigen receptor (CAR) T cells.