日本理化研究所的一個研究小組日前報告說，其科研人員在老鼠實驗中,，成功利用誘導(dǎo)多能干細胞（iPS細胞）大量生成具有抗癌效果的特定淋巴球,，并已確認這種淋巴球被輸入患有癌癥的老鼠體內(nèi)并激活后發(fā)揮了抗癌效果。這種技術(shù)有望在治療癌癥的免疫細胞療法中得到應(yīng)用,。
理化研究所免疫和過敏學綜合研究中心專家渡會浩志率領(lǐng)的研究小組,，在美國《臨床檢查雜志》網(wǎng)絡(luò)版1日登載的論文中指出，NKT細胞是一種淋巴球,，它具有推動其他免疫細胞一起發(fā)揮作用,、直接或間接殺死癌細胞等作用。研究小組從老鼠的脾臟中分離出NKT細胞,，利用病毒向NKT細胞中植入4種基因并將其制成iPS細胞,，爾后再使其全部分化成大量的NKT細胞。
在隨后的研究中,，科研人員給生來沒有NKT細胞的老鼠移植癌細胞,，經(jīng)過一段時間再為其注入用上述方法培育的NKT細胞和活性物質(zhì)，結(jié)果腫瘤就不再生長,，老鼠在植入癌細胞一年后依然生存,。然而在擁有NKT細胞但沒有激活該細胞的對照組中，老鼠在移植癌細胞以后平均1個月就會死亡,。
該研究小組曾與日本千葉大學合作,，開發(fā)出了激活人體內(nèi)NKT細胞，攻擊癌細胞的新免疫細胞療法,。對晚期肺癌患者進行的臨床試驗顯示,，這一新療法取得了更好的效果，但對于生來NKT細胞就少的患者,，療效則要低一些,。因此研究人員設(shè)想，如果增加人體內(nèi)的NKT細胞，抗癌效果就會提高,，但是此前一直沒有大量制造這一特定淋巴球的方法,。
渡會浩志指出，其研究小組正打算以某位癌癥患者的NKT細胞為基礎(chǔ)培育iPS細胞,，制造大量NKT細胞,，爾后將這些NKT細胞輸入該患者體內(nèi)。如果一切順利,，這種方法有望成為更加有效的抗癌療法,。(生物谷Bioon.com)
生物谷推薦原文出處：
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.
