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B7DC/PDL2通过一种不依赖PD-1的机制促进肿瘤免疫。

B7DC/PDL2 promotes tumor immunity by a PD-1-independent mechanism.

作者信息

Liu Xingluo, Gao Jian Xin, Wen Jing, Yin Lijie, Li Ou, Zuo Tao, Gajewski Thomas F, Fu Yang-Xin, Zheng Pan, Liu Yang

机构信息

Department of Pathology, Ohio State University Medical Center, Columbus, OH 43210, USA.

出版信息

J Exp Med. 2003 Jun 16;197(12):1721-30. doi: 10.1084/jem.20022089.

DOI:10.1084/jem.20022089
PMID:12810690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2193953/
Abstract

B7H1 (PDL1) and B7DC (PDL2) are two new members of the B7 family that can interact with PD-1, a putative negative regulator for immune function. Recent studies have provided evidence for inhibitory functions of both members via PD-1. Meanwhile, compelling evidence exists for costimulatory function of both members. Here we demonstrate that expression of B7DC on the tumor cells promotes CD8 T cell-mediated rejection of tumor cells, at both the induction and effector phase of antitumor immunity. Moreover, B7DC binds to PD-1(-/-) cells and enhances T cell killing in a PD-1-independent mechanism. Our results demonstrate a novel pathway for B7DC to promote tumor immunity and may reconcile the apparently contradictory findings on the function of B7DC.

摘要

B7H1（程序性死亡配体1）和B7DC（程序性死亡配体2）是B7家族的两个新成员，它们可与免疫功能的假定负调节因子程序性死亡蛋白1相互作用。最近的研究为这两个成员通过程序性死亡蛋白1发挥抑制功能提供了证据。同时，也有令人信服的证据表明这两个成员具有共刺激功能。在此我们证明，肿瘤细胞上B7DC的表达在抗肿瘤免疫的诱导期和效应期均能促进CD8 T细胞介导的肿瘤细胞排斥反应。此外，B7DC与程序性死亡蛋白1基因敲除（PD-1(-/-)）细胞结合，并通过一种不依赖程序性死亡蛋白1的机制增强T细胞杀伤作用。我们的结果证明了B7DC促进肿瘤免疫的一条新途径，并且可能调和关于B7DC功能的明显矛盾的发现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14d/2193953/5c87d61a0b4e/20022089f8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14d/2193953/0e01397cf97a/20022089f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14d/2193953/2339855f090f/20022089f2.jpg
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Differential expression of PD-L1 and PD-L2, ligands for an inhibitory receptor PD-1, in the cells of lymphohematopoietic tissues.抑制性受体PD-1的配体PD-L1和PD-L2在淋巴造血组织细胞中的差异表达。
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Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion.
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