摘要
B7-H6是近年来发现的新型共刺激分子,在正常细胞无表达,较特异性地表达于肿瘤细胞,并可在炎症状态下诱导表达于抗原呈递细胞,可被去乙酰化酶抑制剂下调表达。B7-H6通过NK细胞表面N Kp30活化NK细胞而杀伤肿瘤及转化细胞,并释放TNFα、IFNγ等细胞因子。细胞表面的B7-H6分子脱落后形成可溶性分子。B7-H6/N Kp30通路可能参与了干燥综合征的发生。因此,B7-16/NKp30通路可能成为肿瘤、炎症、自身免疫性疾病等治疗的新靶点。
B7-H6 is a co-stimulatory molecule discoveried recently.B7-H6 is not expressed on normal cells,but specially expressed on tumor cells.It can also be expressed on antigen presenting cells(APC) by the induction.The B7-H6 expression can be downregulated by HDACi.NK cells can be activated to release TNFα and IFNγ through B7H6-NKp30 pathway.The B7-H6 molecules expressed on the cell surface can be shedded to form soluble molecules.In the meantime,the B7-H6/NKp30 pathway may be involved in the pathogenesis of primary Sjogren syndrome.B7-H6/NKp30 may become a new therapeutic target for tumor,inflammation and autoimmune diseases.This review discusses the B7-H6 and receptor sructure,the expression and significance of B7-H6,the function and regulating mechanism of B74 K and the soluble molecules of B7-H6.
出处
《中国实验血液学杂志》
CAS
CSCD
北大核心
2016年第1期295-298,共4页
Journal of Experimental Hematology
基金
国家自然科学基金资助项目(81172245)