ISSN: 2684-1630
Qing Tan, Wenhui Huang, Yu Zheng, Yueqiang Wen, Mingyan Li, Yi Tao, Shuilian Yu*
Systemic Lupus Erythematosus (SLE) pathogenesis includes a compromised clearance of nucleic acids, increased type I Interferon (IFN) response, dysregulated B cell tolerance causing an increased autoantibody synthesis, immune complex formation and deposition. Autoantigens released because of the defects in regulated cell death pathways could be presented by follicular dendritic cells to autoreactive B cells in Germinal Centers (GCs) resulting in loss of self-tolerance causing production of autoantibodies, immune complexes, and pro-inflammatory cytokines leading to inflammation and tissue damage in SLE. In numerous pathological states in vivo, cells exhibit a variety of active, programmed patterns of cellular necrosis, such as apoptosis, necroptosis, pyroptosis, NETosis, autophagy and ferroptosis. These necrotic cell deaths are generally characterized by cell swelling, rupture of the cell membrane and release of the cell's contents into the surrounding tissues. This review delves into different dysfunction of Regulated Cell Death (RCD), elucidating their roles in SLE progression and offering insights into novel therapeutic avenues.
Published Date: 2025-01-15; Received Date: 2024-03-29