Cutaneous and systemic connections in lupus

Purpose of review Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multiple manifestations, with a majority of SLE patients having cutaneous involvement. Despite ongoing research, the relationship between SLE and cutaneous lupus erythematosus (CLE) pathogeneses remains unknown. This review will compare advances in understanding the cause and pathogenesis of SLE and CLE. Recent findings Recently, mechanisms by which immune cell populations contribute to the pathogenesis of SLE and CLE have been queried. Studies have pointed to transitional B cells and B-cell activating factor (BAFF) signaling as potential drivers of SLE and CLE, with belimumab clinical data supporting these hypotheses. Ustekinumab trials and an exciting regulatory T cell (Treg) adoptive transfer in an SLE patient with cutaneous disease have suggested a role for T-cell-targeted therapies. The theory that neutrophil extracellular traps may be a source of autoantigens in SLE remains controversial, while neutrophils have been suggested as early drivers of cutaneous disease. Finally, plasmacytoid dendritic cells (pDCs) have been studied as a potential therapeutic target in SLE, and anti-blood DC antigen (anti-BDCA) antibody clinical trials have shown promise in treating cutaneous disease. Although recent findings have contributed to understanding SLE and CLE pathogenesis, the mechanistic link between these diseases remains an area requiring further research.