Abstract
Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by excessive inflammatory and immune responses and tissue damage. Increasing evidence has demonstrated the important role of programmed cell death in SLE pathogenesis. When apoptosis encounters with defective clearance, accumulated apoptotic cells lead to secondary necrosis. Different forms of lytic cell death, including secondary necrosis after apoptosis, NETosis, necroptosis, and pyroptosis, contribute to the release of damage-associated molecular patterns (DAMPs) and autoantigens, resulting in triggering immunity and tissue damage in SLE. However, the role of autophagy in SLE pathogenesis is in dispute. This review briefly discusses different forms of programmed cell death pathways and lay particular emphasis on inflammatory cell death pathways such as NETosis, pyroptosis, and necroptosis and their roles in the inflammatory and immune responses in SLE.
Highlights
Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease that affects almost all organs and tissues [1]
Dysregulated cell death in combination with defective clearance of dying cells has been suggested to contribute to the release of damage-associated molecular patterns (DAMPs), amplification of inflammatory and immune responses, production and release of autoantigens, and tissue damage in SLE [6,7,8]
The findings suggest that in SLE enhanced apoptotic cells come across with defective clearance can undergo secondary necrosis/pyroptosis, resulting in autoimmunity that further drive SLE pathogenesis
Summary
Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease that affects almost all organs and tissues [1]. It is characterized by production of abundant autoantibodies, deposition of massive immune complexes, upregulation of inflammatory and immune responses, and damage of different tissues [2]. Dysregulated cell death in combination with defective clearance of dying cells has been suggested to contribute to the release of damage-associated molecular patterns (DAMPs), amplification of inflammatory and immune responses, production and release of autoantigens, and tissue damage in SLE [6,7,8]. We discuss various forms of programmed cell death pathways with particular emphasis on inflammatory cell death such as NETosis, pyroptosis, and necroptosis and their consequences in the inflammatory and immune responses in SLE.
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