血管生成
免疫系统
趋化因子
免疫耐受
癌症研究
生物
缺氧(环境)
免疫学
自身免疫
新生血管
化学
有机化学
氧气
作者
Andrea Facciabene,Xiaohui Peng,Ian S. Hagemann,Klara Balint,Andrea Costantino,Liping Wang,Phyllis A. Gimotty,C. Blake Gilks,Priti Lal,Lin Zhang,George Coukos
出处
期刊:Nature
[Springer Nature]
日期:2011-07-01
卷期号:475 (7355): 226-230
被引量:1160
摘要
Although immune mechanisms can suppress tumour growth, tumours establish potent, overlapping mechanisms that mediate immune evasion. Emerging evidence suggests a link between angiogenesis and the tolerance of tumours to immune mechanisms. Hypoxia, a condition that is known to drive angiogenesis in tumours, results in the release of damage-associated pattern molecules, which can trigger the rejection of tumours by the immune system. Thus, the counter-activation of tolerance mechanisms at the site of tumour hypoxia would be a crucial condition for maintaining the immunological escape of tumours. However, a direct link between tumour hypoxia and tolerance through the recruitment of regulatory cells has not been established. We proposed that tumour hypoxia induces the expression of chemotactic factors that promote tolerance. Here we show that tumour hypoxia promotes the recruitment of regulatory T (T(reg)) cells through induction of expression of the chemokine CC-chemokine ligand 28 (CCL28), which, in turn, promotes tumour tolerance and angiogenesis. Thus, peripheral immune tolerance and angiogenesis programs are closely connected and cooperate to sustain tumour growth.
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