PD-1/B7-H1 interaction contribute to the spontaneous acceptance of mouse liver allograft.
PD-1/B7-H1 interaction contribute to the spontaneous acceptance of mouse liver allograft.
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DOI：
10.1111/j.1600-6143.2009.02859.x
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发表时间：
2010-01
期刊：
影响因子：
--
通讯作者：
Li XK
中科院分区：
文献类型：
--
作者：
Morita M;Fujino M;Jiang G;Kitazawa Y;Xie L;Azuma M;Yagita H;Nagao S;Sugioka A;Kurosawa Y;Takahara S;Fung J;Qian S;Lu L;Li XK
程序性死亡-1（PD-1）/B7-H1通路是免疫应答的重要负调节因子。我们在此研究了PD-1/B7-H1通路在小鼠肝同种异体移植中建立免疫自发耐受状态中的作用。B7-H1在供者来源的组织细胞上高度表达，并且它还与同种异体移植物中浸润的T细胞的凋亡有关。引人注目的是，通过抗B7-H1 mAb或使用B7-H1敲除小鼠作为供体阻断PD-1/B7-H1通路导致严重的细胞浸润以及坏死和坏死，从而导致12天内死亡。此外，与对照组相比，抗体治疗组肝移植物中FasL、穿孔素、颗粒酶B、iNOS和OPN mRNA的表达增加。这些结果提示，B7-H1在肝移植组织细胞上的表达上调在浸润细胞的凋亡中起重要作用，这可能在诱导小鼠肝移植自发耐受中起重要作用。
The programmed death-1 (PD-1)/B7-H1 pathway acts as an important negative regulator of immune responses. We herein investigated the role of the PD-1/B7-H1 pathway in establishing an immunological spontaneous tolerance status in mouse liver allografting. B7-H1 is highly expressed on the donor-derived tissue cells and it is also associated with the apoptosis of infiltrating T cells in the allografts. Strikingly, a blockade of the PD-1/B7-H1 pathway via anti-B7-H1mAb or using B7-H1 knockout mice as a donor led to severe cell infiltration as well as hemorrhaging and necrosis, thus resulting in mortality within 12 days. Furthermore, the expression of the FasL, perforin, granzyme B, iNOS, and OPN mRNA in the liver allografts increased in the antibody-treated group in comparison to the controls. Taken together, these data revealed that the B7-H1 upregulation on the tissue cells of liver allografts thus plays an important role in the apoptosis of infiltrating cells, which might play a critical role of the induction of the spontaneous tolerance after hepatic transplantation in mice.
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DOI：
10.1084/jem.20061577
发表时间：
2006-11-27
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Fife BT;Guleria I;Gubbels Bupp M;Eagar TN;Tang Q;Bour-Jordan H;Yagita H;Azuma M;Sayegh MH;Bluestone JA
通讯作者：
Bluestone JA
影响因子：
30.5
作者：
Latchman, Y;Wood, CR;Freeman, GJ
通讯作者：
Freeman, GJ
影响因子：
13.5
作者：
Yu, MC;Chen, CH;Qian, SG
通讯作者：
Qian, SG
影响因子：
4.4
作者：
Ito, T;Ueno, T;Najafian, N
通讯作者：
Najafian, N
影响因子：
6.2
作者：
Sharland, A;Shastry, S;Bishop, GA
通讯作者：
Bishop, GA