韓國(guó)研究人員3月21日說(shuō),，他們發(fā)現(xiàn)了一種利用結(jié)核桿菌抗癌的新方法,。
這項(xiàng)研究由韓國(guó)釜山大學(xué)醫(yī)學(xué)教授樸永明（音譯）引領(lǐng),，成果發(fā)表在最新一期《癌癥研究》（Cancer Research）雜志上,。
結(jié)核桿菌是導(dǎo)致肺結(jié)核病的“罪魁禍?zhǔn)?rdquo;,。但研究人員從結(jié)核桿菌中成功提取肝素結(jié)合血凝素蛋白，再借助激活樹(shù)突細(xì)胞的方法,，研制出一種有效的治療性癌癥疫苗。
樸永明說(shuō),，實(shí)驗(yàn)鼠接種疫苗后,，體內(nèi)腫瘤明顯減小。
“研究人員知道結(jié)核桿菌突變可用于抗癌或治療糖尿病已有一段時(shí)間,，”樸永明說(shuō),，“但嚴(yán)重的副作用讓人們無(wú)法利用（結(jié)核桿菌治療疾病）。”
不過(guò)他說(shuō),，研究人員發(fā)現(xiàn)的這種抗癌新法能夠“克服這些缺點(diǎn)”,。而且，研究人員利用患癌動(dòng)物體內(nèi)的樹(shù)突細(xì)胞“培育”肝素結(jié)合血凝素蛋白,，可避免患病動(dòng)物機(jī)體產(chǎn)生排異反應(yīng),，有助治療。
樸永明說(shuō),，除可減小腫瘤外,，新疫苗還可在患癌動(dòng)物體內(nèi)“觸發(fā)”積極免疫反應(yīng)，防止癌癥惡化.（生物谷Bioon.com）
生物谷推薦原文出處：
Cancer Research doi: 10.1158/0008-5472.CAN-10-3487
Enhanced efficacy of therapeutic cancer vaccines produced by co-treatment with Mycobacterium tuberculosis heparin-binding hemagglutinin, a novel TLR4 agonist
In Duk Jung1, Soo Kyung Jeong1, Chang-Min Lee2, Kyung Tae Noh2, Deok Rim Heo2, Yong Kyoo Shin3, Cheol-Heui Yun4, Won-Jung Koh5, Shizuo Akira6, Jake Whang7, Hwa-Jung Kim7, Won Sun Park8, Sung Jae Shin7, and Yeong-Min Park9,*
Effective activation of dendritic cells (DCs) towards T helper (Th)-1 cell polarization would improve DC-based antitumor immunotherapy, helping promote the development of immunotherapeutic vaccines based on T cell immunity. To achieve this goal, it is essential to develop effective immune adjuvants that can induce powerful Th1 cell immune responses. The pathogenic organism M. tuberculosis includes certain constitutes, such as heparin-binding hemagglutinin (HBHA), that possess a strong immunostimulatory potential. In this study we report the first clarification of the functions and precise mechanism of HBHA in immune stimulation settings relevant to cancer. HBHA induced DC maturation in a TLR4-dependent manner, elevating expression of the surface molecules CD40, CD80 and CD86, MHC classes I and II and the pro-inflammatory cytokines IL-6, IL-12, IL-1β, TNF-α and CCR7, as well as stimulating the migratory capacity of DCs in vitro and in vivo. Mechanistic investigations established that MyD88 and TRIF signaling pathways downstream of TLR4 mediated secretion of HBHA -induced pro-inflammatory cytokines. HBHA-treated DCs activated na?ve T cells, polarized CD4+ and CD8+ T cells to secrete IFN-γ and induced T cell-mediated cytotoxicity. Notably, systemic administration of DCs that were HBHA-treated and OVA254-267-pulsed ex vivo greatly strengthened immune priming in vivo, inducing a dramatic regression of tumor growth associated with long-term survival in a murine E.G7 thymoma model. Together, our findings highlight HBHA as an immune adjuvant that favors Th1 polarization and DC function for potential applications in DC-based antitumor immunotherapy.
