吡喃结构域
炎症体
炎症
MEFV公司
家族性地中海热
细胞凋亡
促炎细胞因子
免疫学
TLR4型
分子生物学
抗体
生物
医学
基因
内科学
突变
基因突变
遗传学
疾病
作者
Masaaki Shiohara,Shun’ichiro Taniguchi,Junya Masumoto,Kozo Yasui,Kenichi Koike,A Komiyama,Junji Sagara
标识
DOI:10.1016/s0006-291x(02)00384-4
摘要
ASC is an adaptor protein that is composed of two protein-protein interaction domains, a PYRIN domain (PYD), and a caspase-recruitment domain (CARD). Recently, ASC was identified as a binding partner of pyrin, which is the product of MEFV, a gene causing familial Mediterranean fever (FMF). Mutations in MEFV result in defects in control of neutrophil-mediated inflammation. Thus we focused on the expression of ASC in neutrophils. Immunohistochemical study showed that ASC is increased in neutrophils in severe inflammatory sites of gangrenous appendicitis. We, then, tested whether proinflammatory mediators induce ASC using peripheral blood neutrophils in vitro. ASC expression was transiently up-regulated by IL-1alpha, IL-1beta, IFN-alpha, IFN-gamma, TNFalpha, and LPS. ASC was also increased by incubation with either anti-Fas antibody or recombinant soluble Fas ligand. The Fas-mediated induction of ASC was inhibited by a general caspase inhibitor, z-VAD-fmk, and an immunocytochemical study showed that ASC was increased in neutrophils exhibiting characteristic phenotypes for apoptosis. These findings suggest that up-regulation of ASC is closely associated with inflammation and apoptosis in neutrophils.
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