Laboratório de Toxoplasmose e outras Protozooses, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.
Scand J Immunol. 2021 Feb;93(2):e12960. doi: 10.1111/sji.12960. Epub 2020 Sep 8.
Coronavirus disease 2019 (COVID-19) pathogenesis remains under investigation. Growing evidence indicates the establishment of a hyperinflammatory response, characterized by sustained production of cytokines, such as IL-1β. The release and maturation of this cytokine are dependent on the activation of a catalytic multiprotein complex, known as "inflammasome". The most investigated is the NLRP3 inflammasome, which can be activated by various stimuli, such as the recognition of extracellular ATP by the P2X7 receptor. Based on the recent literature, we present evidence that supports the idea that the P2X7R/NLRP3 axis may be involved in the immune dysregulation caused by the SARS-CoV-2 infection.
新型冠状病毒病 2019(COVID-19)的发病机制仍在研究中。越来越多的证据表明,过度炎症反应的建立,其特征是细胞因子如 IL-1β的持续产生。这种细胞因子的释放和成熟依赖于一种称为“炎性体”的催化多蛋白复合物的激活。研究最多的是 NLRP3 炎性体,它可以被各种刺激激活,如 P2X7 受体识别细胞外 ATP。根据最近的文献,我们提出了证据支持这样一种观点,即 P2X7R/NLRP3 轴可能参与了由 SARS-CoV-2 感染引起的免疫失调。