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【medical-news】lancet：癌细胞和微环境对肿瘤免疫
Tumour immunity: effector response to tumour and role of the microenvironment.
Mantovani A, Romero P, Palucka AK, Marincola FM.
Istituto Clinico Humanitas and Institute of Pathology, University of Milan, Milan, Italy.
Substantial evidence shows that inflammation promotes oncogenesis and, occasionally, participates in cancer rejection. This paradox can be accounted for by a dynamic switch from chronic smouldering inflammation promoting cancer-cell survival to florid, tissue-disruptive inflammatory reactions that trigger cancer-cell destruction. Clinical and experimental observations suggest that the mechanism of this switch recapitulates the events associated with pathogen infection, which stimulate immune cells to recognise danger signals and activate immune effector functions. Generally, cancers do not have danger signals and, therefore, they cannot elicit strong immune reactions. Synthetic molecules have been developed that mimic pathogen invasion at the tumour site. These compounds activate dendritic cells to produce proinflammatory cytokines, which in turn trigger cytotoxic mechanisms leading to cancer death. Simultaneously, dendritic cells capture antigen shed by dying cancer cells, undergo activation, and stimulate antigen-specific T and B cells. This process results in massive amplification of the antineoplastic inflammatory process. Thus, although anti-inflammatory drugs can prevent onset of some malignant diseases, induction of T cells specific for tumour antigen by active immunisation, combined with powerful activation signals within the cancer microenvironment, might yield the best strategy for treatment of established cancers.
http://www.thelancet.com/journals/lancet/article/PIIS014067360860241X/pdf 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 由于未见回帖翻译，小弟代为尝试，进行翻译。
Lancet. 2008 Mar 1;371(9614):771-83. Epub 2008 Feb 13.
Tumour immunity: effector response to tumour and role of the microenvironment.
肿瘤免疫：肿瘤与微环境与效应子应答
Substantial evidence shows that inflammation promotes oncogenesis and, occasionally, participates in cancer rejection.
充实的证据表明炎症能够促进肿瘤发生，偶尔也会参与癌症排斥。
This paradox can be accounted for by a dynamic switch from chronic smouldering inflammation promoting cancer-cell survival to florid, tissue-disruptive inflammatory reactions that trigger cancer-cell destruction.
慢性蓄积的炎症促使存活的癌细胞转向鲜红的、组织破坏的炎症反应从而引导癌细胞碎解的动态闸门可以解释这一似是而非的观点。。 学习了。 1.充实的（确切的）证据表明炎症能够促进肿瘤发生。。。
2.临床和试验上的发现（实验的发现）
3.树突状细胞能够捕获死亡的（濒临死亡的）癌细胞释放的抗原，经过（删掉）激活并诱发（刺激）具（删掉）抗原特异性的T细胞和B细胞。
4.这个过程导致了级联放大的抗肿瘤炎症过程（这一方式导致了抗肿瘤炎症过程的级联放大效应）。
5.但自动免疫接种引发的特异性T细胞联合癌瘤微环境中的强活化信号，会让步最有效的针对确诊癌症的方案。（然而，通过主动免疫诱导针对肿瘤抗原的特异性T细胞活化，并结合癌微环境内的强有力的信号的激活，这或许能够给予最佳的方案用于治疗已发生的癌症。）
6.慢性蓄积的炎症促使存活的癌细胞转向鲜红的、组织破坏的炎症反应从而引导癌细胞碎解的动态闸门可以解释这一似是而非的观点。（下面的动态模型或许可用于解释上述悖论，即促使癌细胞存活的慢性蓄积炎症转为发红的组织破坏性的炎症反应，后者可引起癌细胞破坏。）
7. 标题：肿瘤免疫：肿瘤与微环境与效应子应答（肿瘤免疫：肿瘤的应答效应及微环境的作用）
括号内是我的翻译想法，和楼主切磋切磋，呵呵～～，让你见笑了。 修改：1.Tumour immunity: effector response to tumour and role of the microenvironment.(肿瘤免疫：对肿瘤的效应反应和肿瘤微环境的功能)
2.florid, tissue-disruptive inflammatory reactions that trigger cancer-cell destruction 可否翻译为“急性、组织破坏性的炎症反应可促发肿瘤细胞的坏死；
3.Clinical and experimental observations suggest that the mechanism of this switch recapitulates the events associated with pathogen infection, which stimulate immune cells to recognise danger signals and activate immune effector functions. 临床观察和试验研究提示这种转换的机制再现了那些与病原体感染有关联事件，即它们能刺激免疫细胞识别危险信号和活化免疫效应功能。
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作者:admin@医学,生命科学 2011-02-25 17:14
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