1型干扰素受体的IFNAR1链在良性细胞中的表达可预防急性白血病进展。
Expression of the IFNAR1 chain of type 1 interferon receptor in benign cells protects against progression of acute leukemia.
作者信息
Zhao Bin, Bhattacharya Sabyasachi, Yu Qiujing, Fuchs Serge Y
机构信息
a Department of Biomedical Sciences , Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania , Philadelphia , PA , USA.
出版信息
Leuk Lymphoma. 2018 Jan;59(1):171-177. doi: 10.1080/10428194.2017.1319053. Epub 2017 May 15.
Type I interferons (IFN) were widely used for leukemia treatment. These cytokines act on cell surface receptor consisting of the IFNAR1/2 chains to induce anti-tumorigenic effects. Given that levels of IFNAR1 can be regulated by phosphorylation-driven ubiquitination and degradation that undermines IFN signaling and anti-tumorigenic effects, we sought to determine the importance of IFNAR1 downregulation in progression of acute leukemia. Using knock-in mice deficient in downregulation of IFNAR1, we uncovered that IFNAR1 expression in stromal benign cells functions to protect against progression of leukemia. We discuss putative mechanisms of this regulation and potential of therapeutic targeting of IFNAR1 downregulation to treat leukemia.
I型干扰素（IFN）曾被广泛用于白血病治疗。这些细胞因子作用于由IFNAR1/2链组成的细胞表面受体，以诱导抗肿瘤作用。鉴于IFNAR1的水平可通过磷酸化驱动的泛素化和降解来调节，而这会破坏IFN信号传导和抗肿瘤作用，我们试图确定IFNAR1下调在急性白血病进展中的重要性。利用缺乏IFNAR1下调功能的基因敲入小鼠，我们发现基质良性细胞中的IFNAR1表达具有预防白血病进展的作用。我们讨论了这种调节的假定机制以及靶向IFNAR1下调进行治疗白血病的潜力。
Zotero 插件