上睑下垂
炎症体
促炎细胞因子
生物
半胱氨酸蛋白酶
溶解循环
细胞生物学
分泌物
程序性细胞死亡
免疫学
白细胞介素18
炎症
半胱氨酸蛋白酶1
细胞凋亡
细胞因子
遗传学
生物化学
病毒
作者
Mohamed Lamkanfi,Vishva M. Dixit
出处
期刊:Cell
[Elsevier]
日期:2014-05-01
卷期号:157 (5): 1013-1022
被引量:2110
标识
DOI:10.1016/j.cell.2014.04.007
摘要
Recent studies have offered a glimpse into the sophisticated mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1β and IL-18. Activation of caspases 1 and 11 in canonical and noncanonical inflammasomes, respectively, also protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell death. The therapeutic potential of inhibiting these proinflammatory caspases in infectious and autoimmune diseases is raised by the successful deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant inflammasome signaling. This Review summarizes recent insights into inflammasome biology and discusses the questions that remain in the field. Recent studies have offered a glimpse into the sophisticated mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1β and IL-18. Activation of caspases 1 and 11 in canonical and noncanonical inflammasomes, respectively, also protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell death. The therapeutic potential of inhibiting these proinflammatory caspases in infectious and autoimmune diseases is raised by the successful deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant inflammasome signaling. This Review summarizes recent insights into inflammasome biology and discusses the questions that remain in the field.
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