日本理化研究所的一个研究小组日前报告说，其科研人员在老鼠实验中，成功利用诱导多能干细胞（iPS细胞）大量生成具有抗癌效果的特定淋巴球，并已确认这种淋巴球被输入患有癌症的老鼠体内并激活后发挥了抗癌效果。这种技术有望在治疗癌症的免疫细胞疗法中得到应用。
理化研究所免疫和过敏学综合研究中心专家渡会浩志率领的研究小组，在美国《临床检查杂志》网络版1日登载的论文中指出，NKT细胞是一种淋巴球，它具有推动其他免疫细胞一起发挥作用、直接或间接杀死癌细胞等作用。研究小组从老鼠的脾脏中分离出NKT细胞，利用病毒向NKT细胞中植入4种基因并将其制成iPS细胞，尔后再使其全部分化成大量的NKT细胞。
在随后的研究中，科研人员给生来没有NKT细胞的老鼠移植癌细胞，经过一段时间再为其注入用上述方法培育的NKT细胞和活性物质，结果肿瘤就不再生长，老鼠在植入癌细胞一年后依然生存。然而在拥有NKT细胞但没有激活该细胞的对照组中，老鼠在移植癌细胞以后平均1个月就会死亡。
该研究小组曾与日本千叶大学合作，开发出了激活人体内NKT细胞，攻击癌细胞的新免疫细胞疗法。对晚期肺癌患者进行的临床试验显示，这一新疗法取得了更好的效果，但对于生来NKT细胞就少的患者，疗效则要低一些。因此研究人员设想，如果增加人体内的NKT细胞，抗癌效果就会提高，但是此前一直没有大量制造这一特定淋巴球的方法。
渡会浩志指出，其研究小组正打算以某位癌症患者的NKT细胞为基础培育iPS细胞，制造大量NKT细胞，尔后将这些NKT细胞输入该患者体内。如果一切顺利，这种方法有望成为更加有效的抗癌疗法。(生物谷Bioon.com)
生物谷推荐原文出处：
J Clin Invest. doi:10.1172/JCI39896.
Sonic hedgehog is a critical mediator of erythropoietin-induced cardiac protection in mice
Kazutaka Ueda1, Hiroyuki Takano1, Yuriko Niitsuma1,2, Hiroshi Hasegawa1, Raita Uchiyama1, Toru Oka1, Masaru Miyazaki2, Haruaki Nakaya3 and Issei Komuro1
1Department of Cardiovascular Science and Medicine,
2Department of General Surgery, and
3Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan.
Erythropoietin reportedly has beneficial effects on the heart after myocardial infarction, but the underlying mechanisms of these effects are unknown. We here demonstrate that sonic hedgehog is a critical mediator of erythropoietin-induced cardioprotection in mice. Treatment of mice with erythropoietin inhibited left ventricular remodeling and improved cardiac function after myocardial infarction, independent of erythropoiesis and the mobilization of bone marrow–derived cells. Erythropoietin prevented cardiomyocyte apoptosis and increased the number of capillaries and mature vessels in infarcted hearts by upregulating the expression of angiogenic cytokines such as VEGF and angiopoietin-1 in cardiomyocytes. Erythropoietin also increased the expression of sonic hedgehog in cardiomyocytes, and inhibition of sonic hedgehog signaling suppressed the erythropoietin-induced increase in angiogenic cytokine expression. Furthermore, the beneficial effects of erythropoietin on infarcted hearts were abolished by cardiomyocyte-specific deletion of sonic hedgehog. These results suggest that erythropoietin protects the heart after myocardial infarction by inducing angiogenesis through sonic hedgehog signaling.
