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Systemic lupus erythematosus is systemic autoimmune disease characterized by a wide range of clinical manifestations, from skin and mucosal lesions to severe injuries in the central nervous system, kidneys and other organs. The presence of high titres of autoantibodies against nuclear components, immune complexes deposition, complement deficiency and lymphocytes infiltration in affected tissues, which causes tissue and organ damage are the main characteristics of the disease. Nowadays, many studies elucidate the essential role of autophagy in the occurrence, development and severity of systemic lupus erythematosus.
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Autophagy is a highly conserved lysosome-mediated catabolic process. It can remove unwanted cytoplasmic components, such as long-lived and/or misfolded proteins, damaged organelles, playing an important role in maintaining cellular homeostasis and cell survival in stress conditions, such as nutrient deprivation and hypoxia.
Recently, Autophagy is implicated in nearly all steps of both innate and adaptive immune responses, including neutrophil extracellular trap and inflammasome formation, pathogen recognition, lymphocyte and monocyte development and function, antigen processing and presentation, type I interferon production and inflammatory regulation, thus playing an important part in maintaining the balance of immune system.
Autophagy is divided into three major types: macroautophagy, microautophagy, and chaperone-mediated autophagy, with macroautophagy being the most investigated and understood. Disturbances in autophagy have been implicated in chronic inflammatory diseases and several autoimmune diseases, including Systemic lupus erythematosus, multiple sclerosis, Crohn's disease and rheumatoid arthritis.
Several regulatory factors that may play key roles in autophagy processes have been discovered in recent years, such as beclin1, which is the key regulatory factor in the autophagy startup process, microtubule-associated protein-light chain 3, autophagy-related gene 5, which are components of autophagosomes.
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100 participants in 2 patient groups
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Mohamed Ali el-feky, prof; Mohamed Saad Badary, prof
Data sourced from clinicaltrials.gov
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