Mig, the monokine induced by interferon-gamma, promotes tumor necrosis in vivo
Mig, the monokine induced by interferon-gamma, promotes tumor necrosis in vivo
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DOI：
10.1182/blood.v89.8.2635
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发表时间：
1997-04-15
期刊：
影响因子：
20.3
通讯作者：
Tosato, G
中科院分区：
文献类型：
--
作者：
Sgadari, C;Farber, JM;Tosato, G
Mig 是由干扰素 γ 诱导的单因子，是一种 CXC 趋化因子，可作为活化 T 细胞的趋化剂。 Mig 在功能上与干扰素诱导蛋白 10 (IP-10) 相关，并与干扰素诱导蛋白 10 (IP-10) 共享受体 CXCR3，此前发现 IP-10 具有体内抗肿瘤活性，在本研究中，发现与进行性生长的肿瘤相比，在裸鼠中建立的伯基特淋巴瘤消退肿瘤中，小鼠 Mig RNA 的表达水平更高，每日接种纯化的重组人 将米格放入裸鼠皮下生长的伯基特肿瘤中，始终会引起与广泛血管损伤相关的肿瘤坏死。这些效果与用 IP-10 瘤内接种 Burkitt 肿瘤所产生的效果没有区别。这些结果支持 Mig 与 IP-10 一样具有体内抗肿瘤活性的观点。这是美国政府的一项工作。
Mig, the monokine induced by interferon-gamma, is a CXC chemokine active as a chemoattractant for activated T cells. Mig is related functionally to interferon-inducible protein 10 (IP-10), with which it shares a receptor, CXCR3, Previously, IP-10 was found to have antitumor activity in vivo, In the present study, murine Mig RNA was found to be expressed at higher levels in regressing Burkitt's lymphoma tumors established in nude mice compared with progressively growing tumors, Daily inoculations of purified recombinant human Mig into Burkitt's tumors growing subcutaneously in nude mice consistently caused tumor necrosis associated with extensive vascular damage. These effects were indistinguishable from those produced by intratumor inoculations of Burkitt's tumors with IP-10, These results support the notion that Mig, like IP-10, has antitumor activity in vivo, This is a US government work.