Since the first textbook devoted to cytokine storm syndromes (CSSs) was published in 2019, the world has changed dramatically and the term’s visibility has broadened. Herein, we define CSSs broadly to include life/organ-threatening systemic inflammation and immunopathology regardless of the context in which it occurs, recognizing that the indistinct borders of such a definition limit its utility. Nevertheless, we are focused on the pathomechanisms leading to CSSs, including impairment of granule-mediated cytotoxicity, specific viral infections, excess IL-18, and chimeric antigen receptor T-cell therapy. These mechanisms are often reflected in distinct clinical features, functional tests, and/or biomarker assessments. Moreover, these mechanisms often indicate specific, definitive treatments. This mechanism-focused organization is vital to both advancing the field and understanding the complexities in individual patients. However, increasing evidence suggests that these mechanisms interact and overlap. Likewise, the utility of a broad term such as “cytokine storm” is that it reflects a convergence on a systemic inflammatory phenotype that, regardless of cause or context, may be amenable to “inflammo-stabilization.” CSS research must improve our appreciation of its various mechanisms and their interactions and treatments, but it must also identify the signs and interventions that may broadly prevent CSS-induced immunopathology.

自 2019 年出版第一本专门研究细胞因子风暴综合征 (CSSs) 的教科书以来，世界发生了巨大变化，该术语的知名度扩大了。在这里，我们将 CSS 广义地定义为包括威胁生命/器官的全身性炎症和免疫病理学，无论其发生的背景如何，认识到这种定义的模糊边界限制了其效用。然而，我们专注于导致 CSSs 的病理机制，包括颗粒介导的细胞毒性受损、特定病毒感染、过量 IL-18 和嵌合抗原受体 T 细胞治疗。这些机制通常反映在不同的临床特征、功能测试和/或生物标志物评估中。此外，这些机制通常表明特定的、确定的治疗方法。这种以机制为中心的组织对于推进该领域和了解个体患者的复杂性至关重要。然而，越来越多的证据表明这些机制相互作用和重叠。同样，“细胞因子风暴”等广义术语的效用在于它反映了系统性炎症表型的趋同，无论原因或背景如何，都可能适用于“炎症稳定”。CSS 研究必须提高我们对其各种机制及其相互作用和治疗的认识，但它还必须确定可能广泛预防 CSS 诱导的免疫病理学的迹象和干预措施。诸如“细胞因子风暴”之类的广义术语的用途在于，它反映了系统性炎症表型的趋同，无论原因或背景如何，都可能适用于“炎症稳定”。CSS 研究必须提高我们对其各种机制及其相互作用和治疗的认识，但它还必须确定可能广泛预防 CSS 诱导的免疫病理学的迹象和干预措施。诸如“细胞因子风暴”之类的广义术语的用途在于，它反映了系统性炎症表型的趋同，无论原因或背景如何，都可能适用于“炎症稳定”。CSS 研究必须提高我们对其各种机制及其相互作用和治疗的认识，但它还必须确定可能广泛预防 CSS 诱导的免疫病理学的迹象和干预措施。