解析NALP-3/白细胞介素-1β炎性小体：从小突变中获得的重大启示。
Unraveling the NALP-3/IL-1beta inflammasome: a big lesson from a small mutation.
作者信息
Dinarello Charles A
机构信息
University Colorado Health Sciences Center, Division of Infectious Diseases, B168, 4200 East Ninth Avenue, Denver, CO 80262, USA.
出版信息
Immunity. 2004 Mar;20(3):243-4. doi: 10.1016/s1074-7613(04)00055-x.
Abstract
Cytokine-mediated inflammation is a target for novel therapies as well as for fundamental research. A single amino acid mutation in the NALP-3 gene controlling the activation of caspase-1 results in increased processing of the inactive IL-1beta precursor and release of the active cytokine. Blocking IL-1 receptors arrests inflammation in humans with the mutation.
摘要
细胞因子介导的炎症是新型疗法以及基础研究的靶点。控制半胱天冬酶-1激活的NALP-3基因中的单个氨基酸突变会导致无活性的白细胞介素-1β前体的加工增加以及活性细胞因子的释放。阻断白细胞介素-1受体可使携带该突变的人类炎症停止。
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