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Systemic lupus erythematosus (SLE) is the tenth leading cause of death infemales 15-24 years old in the US. The diversity of symptoms and immunepathways expressed in SLE patients causes difficulties in treating SLE as wellas in new clinical trials. This study used unsupervised learning on geneexpression data from adult SLE patients to separate patients into clusters. Thedimensionality of the gene expression data was reduced by three separatemethods (PCA, UMAP, and a simple linear autoencoder) and the results from eachof these methods were used to separate patients into six clusters with k-meansclustering.  The clusters revealed three separate immune pathways in the SLE patients thatcaused SLE. These pathways were: (1) high interferon levels, (2) highautoantibody levels, and (3) dysregulation of the mitochondrial apoptosispathway. The first two pathways have been extensively studied in SLE. However,mitochondrial apoptosis has not been investigated before to the best of ourknowledge as a standalone cause of SLE, independent of autoantibody production,indicating that mitochondrial proteins could lead to a new set of therapeutictargets for SLE in future research.

Stratification of Systemic Lupus Erythematosus Patients Using Gene Expression Data to Reveal Expression of Distinct Immune Pathways