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<p>Neutrophils are granular and polymorphonuclear cells and one of the main participants of the innate immune system, which have received considerable attention due to the discovery of neutrophil extracellular traps (NETs). Extracellular vesicles (EVs), particularly those released by immune cells such as neutrophils, have been associated with the immunopathogenesis of autoimmune diseases. Besides, studies have reported a fundamental correlation between EVs and NETosis in autoimmune diseases. Neutrophil-generated NET-derived EVs contain various cargos, especially autoantigens that either promote inflammation or cause tissue damage, thereby triggering the initiation or progression. The NETs-EVs pathogenic correlation involved in the immunopathogenesis of autoimmune diseases could provide therapeutic opportunities through approaches such as blocking neutrophil-generated NET formation and inhibiting NET-derived EV secretion. Determining the underlying mechanism by which NETs-EVs correlation participates in autoimmune disease pathogenesis may lead to identifying novel and specific therapeutic approaches.</p>

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A comprehensive insight into NETosis-extracellular vesicle crosstalk in autoimmune diseases

  • 期刊论文

  • 发表日期：

    2025年9月6日

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  • Mohammed Hashim Mohammed,
  • Sumaya Ayad Abdulrazzaq,
  • Aysar Ashour Khalaf,
  • Ashok Kumar Bishoyi,
  • Roopashree R,
  • Aditya Kashyap,
  • Kamal Kant Joshi,
  • Arshed Shakir Kadim,
  • Muthena Kariem,
  • Abed J. Kadhim

摘要

Neutrophils are granular and polymorphonuclear cells and one of the main participants of the innate immune system, which have received considerable attention due to the discovery of neutrophil extracellular traps (NETs). Extracellular vesicles (EVs), particularly those released by immune cells such as neutrophils, have been associated with the immunopathogenesis of autoimmune diseases. Besides, studies have reported a fundamental correlation between EVs and NETosis in autoimmune diseases. Neutrophil-generated NET-derived EVs contain various cargos, especially autoantigens that either promote inflammation or cause tissue damage, thereby triggering the initiation or progression. The NETs-EVs pathogenic correlation involved in the immunopathogenesis of autoimmune diseases could provide therapeutic opportunities through approaches such as blocking neutrophil-generated NET formation and inhibiting NET-derived EV secretion. Determining the underlying mechanism by which NETs-EVs correlation participates in autoimmune disease pathogenesis may lead to identifying novel and specific therapeutic approaches.