日本的一個(gè)研究小組在新一期《自然—醫(yī)學(xué)》雜志網(wǎng)絡(luò)版上報(bào)告說,，干擾素能控制作為血細(xì)胞源頭的造血干細(xì)胞的作用,，組合使用干擾素和抗癌劑或許能創(chuàng)造出一種效果好且副作用小的白血病治療方法。
干擾素是一種廣譜抗病毒劑,，這種物質(zhì)主要通過細(xì)胞表面受體作用使細(xì)胞產(chǎn)生抗病毒蛋白,，從而抑制病毒復(fù)制。目前,，干擾素常被用于治療肝炎等病,。
來自東京醫(yī)科齒科大學(xué)和秋田大學(xué)的研究人員給實(shí)驗(yàn)鼠注入能令它們體內(nèi)產(chǎn)生干擾素的物質(zhì)，然后分析實(shí)驗(yàn)鼠造血干細(xì)胞的變化,。他們發(fā)現(xiàn),，如果短時(shí)間注入這種物質(zhì)，造血干細(xì)胞就會(huì)增殖,，而一旦持續(xù)注入這種物質(zhì),，實(shí)驗(yàn)鼠體內(nèi)的造血干細(xì)胞又會(huì)減少。這表明,，干擾素能夠左右造血干細(xì)胞的作用,。
在慢性骨髓性白血病患者體內(nèi)，存在一種類似造血干細(xì)胞的白血病干細(xì)胞,，這種干細(xì)胞能產(chǎn)生白血病細(xì)胞,。用抗癌劑治療白血病的時(shí)候，由于抗癌劑只對(duì)增殖中的細(xì)胞能充分發(fā)揮效用,，而白血病干細(xì)胞又容易進(jìn)入休眠狀態(tài),，所以抗癌劑的效果常常不能完全發(fā)揮，這也是白血病容易復(fù)發(fā)的原因,。
而上述新研究表明,，短時(shí)間給予干擾素能激活造血干細(xì)胞。研究人員認(rèn)為,，可以利用這一機(jī)制,，在實(shí)施抗癌劑治療前，先用干擾素激活白血病干細(xì)胞,，這樣就有可能提高抗癌劑的效果,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Medicine 31 May 2009 | doi:10.1038/nm.1973
Interferon regulatory factor-2 protects quiescent hematopoietic stem cells from type I interferon–dependent exhaustion
Taku Sato1,2, Nobuyuki Onai1,2, Hiroki Yoshihara3, Fumio Arai3, Toshio Suda3 & Toshiaki Ohteki1,2,4
Type I interferons (IFNs), a family of cytokines, orchestrate numerous biological and cellular processes1, 2, 3. Although it is well known that type I IFNs are essential for establishing the host antiviral state4, their role in hematopoietic homeostasis has not been studied. Here we show that type I IFNs induce proliferation and exhaustion in hematopoietic stem cells (HSCs) and that interferon regulatory factor-2 (IRF2), a transcriptional suppressor of type I IFN signaling5, 6, preserves the self-renewal and multilineage differentiation capacity of HSCs. HSCs were substantially less abundant in the bone marrow of Irf2-/- as compared to Irf2+/- mice. Irf2-/- HSCs showed enhanced cell cycling status and failed to produce hematopoietic cells in competitive repopulation assays, and the reconstituting capacity of Irf2-/- HSCs was restored by disabling type I IFN signaling in these cells. In wild-type mice, injection of poly(I:C), an inducer of type I IFN signaling, or IFN- induced HSC proliferation, and chronic type I IFN signaling further reduced the number of quiescent HSCs. Notably, combined poly(I:C) and 5-fluorouracil (5-FU) treatment allowed exogenous HSC engraftment and hematopoietic reconstitution in WT mice. Our findings provide insight into the molecular basis for the maintenance of HSC quiescence and may lead to improvements in bone marrow transplantation and type I IFN–based therapies for viral infection and cancer.
1 Department of Immunology, Akita University Graduate School of Medicine, Akita, Japan.
2 Japan Science and Technology Agency, Core Research for Evolutional Science and Technology (CREST), Tokyo, Japan.
3 Department of Cell Differentiation, The Sakaguchi Laboratory of Developmental Biology, Keio University School of Medicine, Tokyo, Japan.
4 Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
