Cytokine storm syndrome (CSS) has generally been described as a collection of clinical manifestations resulting from an overactivated immune system. Cytokine storms (CSs) are associated with various pathologies, as observed in infectious diseases, certain acquired or inherited immunodeficiencies and autoinflammatory diseases, or following therapeutic interventions. Despite the role of CS in tissue damage and multiorgan failure, a systematic understanding of its underlying molecular mechanisms is lacking. Recent studies demonstrate a positive feedback loop between cytokine release and cell death pathways; certain cytokines, pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs), can activate inflammatory cell death, leading to further cytokine secretion. Here, we discuss recent progress in innate immunity and inflammatory cell death, providing insights into the cellular and molecular mechanisms of CSs and therapeutics that might quell ensuing life-threatening effects.

细胞因子风暴综合征 (CSS) 通常被描述为由过度激活的免疫系统引起的一系列临床表现。细胞因子风暴 (CSs) 与各种病理相关，如在传染病、某些获得性或遗传性免疫缺陷和自身炎症性疾病或治疗干预后观察到的。尽管 CS 在组织损伤和多器官衰竭中发挥作用，但仍缺乏对其潜在分子机制的系统理解。最近的研究表明细胞因子释放和细胞死亡途径之间存在正反馈循环；某些细胞因子、病原体相关分子模式 (PAMP) 和损伤相关分子模式 (DAMP) 可以激活炎症细胞死亡，导致进一步的细胞因子分泌。这里，