| 英文摘要 |
Polymorphonuclear neutrophils (PMNs) are traditionally regarded as the body’s defense cells for phagocytosis and killing of microbes. However, recent investigations have revealed that PMNs are highly heterogeneous and sophisticated phagocytes that can play a variety of inflammatory, immunological, cancer‑regulatory, and autoimmune‑modulatory activities under different pathological milieus in the body. The manifold functions and heterogeneity of PMNs are recognized as N1 (immunostimulatory) and N2 (immunosuppressive) subsets or N0 (pro‑cancerous) and N2 (anti‑cancerous) subsets in autoimmune diseases and malignant neoplasms. In addition, PMNs in certain autoimmune diseases can also be classified into low‑density granulocytes (LDGs) representing pro‑inflammatory neutrophils and high‑density granulocytes (Gr‑1high or CD177+) exhibiting anti‑inflammatory activities. Regarding their multiple regulatory roles on innate and adaptive immunity via neutrophil extracellular trap (NET) release, the evolving of LDG and the liberation of cytokines, we’ll focus on the roles of normal and/or abnormal PMN functions in the pathogenesis and immunopathology of the representative autoimmune rheumatic diseases, rheumatoid arthritis and systemic lupus erythematosus. Collectively, production of rheumatoid factors, delayed NET clearance, and overactivity of peptidylarginine deiminase 4 are the hub for rheumatoid pathogenesis. On the other hand, abnormal cytokine production, increased LDG proliferation, and deoxyribonuclease dysfunction are the crucial factors for lupus pathogenesis. |
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