Immune Profiling of Systemic Lupus Erythematosus

Abstract

Studies in animal models and lupus patients suggest several mechanisms driving the loss of B cell regulation in Systemic Lupus Erythematosus (SLE). The first mechanism involves the overexpression of B cell activating factor and the second is driven by follicular T helper (Tfh) cells. Monocytes have been implicated in the pathogenesis of SLE through recognition of immune complexes containing TLR-binding self-antigens. The overall decrease of NK cells and increase of CD56briCD16- NK cells could further promote immune dysregulation in SLE. Our aim was to determine whether these abnormalities co-exist within each patient, or if human SLE can be subcategorised depending on the immune process driving the disease. We found that NK cells, CD4+ T cells and Tfh cells were decreased and lymphocytes, atypical memory B cells and CD56briCD16- NK cells were increased in SLE. Analysis with the complete data set showed no individual signatures of SLE but we could distinguish SLE patients from those without SLE based on the variables measured in the study. We developed models for predicting if an individual has SLE, if an SLE patient has renal involvement and predicting SLE Disease Activity Index, forming the basis for improved diagnosis and assessment of SLE in the future.