Pathological mechanisms and crosstalk among different forms of cell death in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder characterized by a profound immune dysregulation and the presence of a variety of autoantibodies. Aberrant activation of programmed cell death (PCD) signaling and accelerated cell death is critical in the immunopathogenesis of SLE. Accumulating cellular components from the dead cells and ineffective clearance of the dead cell debris, in particular the nucleic acids and nucleic acids-protein complexes, provide a stable source of self-antigens, which potently activate auto -reactive B cells and promote IFN-I responses in SLE. Different cell types display distinct susceptibility and characteristics to a certain type of cell death, while different PCDs in various cells have mutual and intricate connections to promote immune dysregulation and contribute to the development of SLE. In this review, we discuss the role of various cell death pathways and their interactions in the pathogenesis of SLE. An in depth understanding of the interconnections among various forms cell death in SLE will lead to a better understanding of disease pathogenesis, shedding light on the development of novel therapeutic targets.

Automated summary

SLE is a systemic autoimmune disorder characterized by immune dysregulation and presence of autoantibodies. Aberrant activation of programmed cell death signaling and accelerated cell death is critical in the immunopathogenesis of SLE, providing stable source of self-antigens. Different cell types display distinct susceptibility and characteristics to cell death, while different cell death forms in various cells have intricate connections promoting immune dysregulation and contributing to the development of SLE.