Hou Jinxiu, Zheng Yi, Gao Chengjiang
Key Laboratory of Infection and Immunity, Shandong Province & Key Laboratory for Experimental Teratology, Ministry of Education, Shandong University, Jinan 250012, China.
Department of Immunology, the School of Basic Medical Sciences, Shandong University, Jinan 250012, China.
Biophys Rep. 2023 Dec 31;9(6):338-351. doi: 10.52601/bpr.2023.230032.
During the COVID-19 pandemic, the interplay between the processes of immunity and senescence is drawing more and more intensive attention. SARS-CoV-2 infection induces senescence in lung cells, failure to clear infected cells and increased presence of inflammatory factors could lead to a cytokine storm and acute respiratory disease syndrome (ARDS), which together with aging and age-associated disease lead to 70% of COVID-19-related deaths. Studies on how senescence initiates upon viral infection and how to restrict excessive accumulation of senescent cells to avoid harmful inflammation are crucially important. Senescence can induce innate immune signaling, and innate immunity can engage cell senescence. Here, we mainly review the innate immune pathways, such as cGAS-STING, TLRs, NF-κB, and NLRP3 inflammasome, participating in the senescence process. In these pathways, IFN-I and inflammatory factors play key roles. At the end of the review, we propose the strategies by which we can improve the immune function and reduce inflammation based on these findings.
在新冠疫情期间，免疫与衰老过程之间的相互作用正受到越来越密切的关注。新型冠状病毒2（SARS-CoV-2）感染会诱导肺细胞衰老，无法清除受感染细胞以及炎症因子的增加会导致细胞因子风暴和急性呼吸窘迫综合征（ARDS），这与衰老及年龄相关疾病共同导致了70%的新冠相关死亡病例。研究病毒感染后衰老如何启动以及如何限制衰老细胞的过度积累以避免有害炎症至关重要。衰老可诱导先天性免疫信号传导，而先天性免疫也可引发细胞衰老。在此，我们主要综述参与衰老过程的先天性免疫途径，如cGAS-STING、Toll样受体（TLRs）、核因子κB（NF-κB）和NLRP3炎性小体。在这些途径中，I型干扰素（IFN-I）和炎症因子发挥关键作用。在综述结尾，我们基于这些发现提出了可改善免疫功能并减轻炎症的策略。
