期刊
ANNUAL REVIEW OF IMMUNOLOGY, VOL 29
卷 29, 期 -, 页码 707-735出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-031210-101405
关键词
innate immunity; metabolic diseases; cancer; IL-1 beta; caspase-1
类别
资金
- NCI NIH HHS [R21CA131645, R21 CA131645] Funding Source: Medline
- NIAID NIH HHS [R01 AI063031, U54 AI057157, R01-AI063031, U54-AI057157] Funding Source: Medline
- NIDCR NIH HHS [R01-DE018281, R01-DE016326, R01 DE016326, R01 DE018281] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R21CA131645] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U54AI057157, R01AI063031] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE018281] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE016326] Funding Source: NIH RePORTER
Inflammasome activation leads to caspase-1 activation, which causes the maturation and secretion of pro-IL-1 beta and pro-IL-18 among other substrates. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoinumine disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据