中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2011, 23(5): 440-444
Api6/AIM/Spα调节免疫和脂质代谢的生物学功能研究
方 严,刘 丹,练雪梅*
(重庆医科大学感染性疾病分子生物学教育部重点实验室脂质研究中心,重庆医科大学公共卫生学院营养与食品卫生学教研室,重庆 400016)
摘 要:凋亡抑制因子6(apoptosis inhibitor 6, Api6),又称作AIM/Spα,是清道夫受体富含半胱氨酸残基超家族新成员。Api6/AIM/Spα由巨噬细胞特异性表达,具有抑制CD4+/CD8+双阳性胸腺细胞、T淋巴细胞、NKT淋巴细胞和巨噬细胞凋亡的作用。作为模式识别受体,Api6/AIM/Spα直接与病原体相关分子模式LPS/LTA结合,在机体固有免疫和适应性免疫中发挥重要的作用。近年研究发现,Api6/AIM/Spα可以通过抑制动脉粥样硬化斑块部位巨噬细胞凋亡加重动脉粥样硬化早期斑块的进展,也可以通过抑制脂肪酸合成酶(FAS)的生物学活性提高脂肪细胞的脂解作用,在肥胖的进展中发挥重要作用。重点综述了Api6/AIM/Spα调节免疫和脂质代谢等生物学功能的研究进展。
关键词:凋亡抑制因子6;清道夫受体;细胞凋亡;肝X受体;脂代谢
 
Progress in biological function of Api6/AIM/Spα in immune regulation and lipid metabolism
FANG Yan, LIU Dan, LIAN Xue-Mei*
(Centre for Lipid Research, Key Laboratory of Molecular Biology on Infectious Disease, Ministry of Education; Department of Nutrition and Food Hygiene, School of Public Health, Chongqing Medical University, Chongqing 400016, China)
Abstract: Apoptosis inhibitor 6(Api6), also known as AIM and Spα, belongs to the scavenger receptor cysteine rich-superfamily (SRCR-SF). Api6/AIM/Spα, which is secreted exclusively by macrophages, inhibits apoptosis of CD4/CD8 double-positive (CD4+/CD8+) thymocytes, T cells, natural killer T(NKT) cells and macrophags. As a pattern recognition receptor, Api6/AIM/Spα is involved in the recognition of pathogen-associated molecular patterns(e.g. LPS and LTA), which suggests that it plays an important role in the regulation of the innate and adaptive immune systems. It has been confirmed recently that Api6/AIM/Spα increases early atherosclerotic lesion development by decreasing macrophage apoptosis. Api6/AIM/Spα also associates with cytosolic fatty acid synthase (FAS), decreases FAS activity, thereby inducing the lipolytic response within adipocytes and is physiologically relevanting to obesity progression. This paper introduced emphatically the progress in biological function of Api6/AIM/Spα in immune regulation and lipid metabolism.
Key words: Api6/AIM/Spα; scavenger receptor; apoptosis; LXR; lipid metabolism
 
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