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共刺激分子B7-H1参与肿瘤免疫的研究进展 被引量：4

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摘要 B7-H1是继B7-1和B7-2之后发现的第3个B7家族分子。B7-H1可以抑制T淋巴细胞的增殖分化,促进调节性T细胞(Treg)的分化以及抑制性细胞因子的分泌,从而抑制免疫应答。B7-H1高表达于多种肿瘤细胞表面,它可通过与肿瘤浸润淋巴细胞上的相应受体结合,诱导淋巴细胞凋亡。因此高表达于肿瘤细胞的B7-H1可能参与了肿瘤的免疫逃逸过程。B7-Hl在肿瘤组织中的表达水平和肿瘤患者的临床病理特征及预后紧密相关。此外,B7-H1也参与上皮间质转化过程,提示该分子还可能与肿瘤的发生和转移有关。通过靶向干预B7-H1通路,有望重建肿瘤浸润淋巴细胞对肿瘤的免疫应答,抑制肿瘤的生长和转移,从而达到治疗肿瘤的目的,这一策略在临床实验中也取得了不错的效果。
作者 王琪 杨安钢 温伟红
机构地区 第四军医大学口腔医学系六队 第四军医大学肿瘤生物学国家重点实验室 第四军医大学免疫学教研室
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2013年第4期437-440,共4页 Chinese Journal of Cellular and Molecular Immunology
基金 国家自然科学基金(81171924)
关键词 B7-H1 肿瘤免疫逃逸 抗体治疗 免疫调节
分类号 R392.11 [医药卫生—免疫学]
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参考文献6

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共引文献44

同被引文献68

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细胞与分子免疫学杂志
2013年 第4期

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