P Musiani, A Modesti, M Brunetti, A Modica, P Vitullo, A Gulino, M C Bosco, M P Colombo, P Nanni, F Cavallo
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引用次数: 0
摘要
用小鼠白细胞介素(IL)-2、IL-4和干扰素(IFN)- γ基因转导BALB/c小鼠的自发性乳腺腺癌。与TS/A亲本细胞(TS/A-pc)和单独转导新霉素耐药基因的细胞相比,在sc攻击后释放IL-2、IL-4或ifn - γ的克隆形成肿瘤的能力进行了比较。细胞因子基因转导克隆激活了强烈的炎症反应。由IL-2和il -4基因转导的细胞所引发的肿瘤排斥反应是有效的。这种反应依赖于几种细胞机制的激活,那些被归类为非特异性的是主要的。在反应中招募的反应性白细胞的数量随分泌的细胞因子的功能而变化。克隆排斥后继发对侧TS/ a -pc刺激的生长明显受损。
Nature and potential of the reactive response to mouse mammary adenocarcinoma cells engineered with interleukin-2, interleukin-4 or interferon-gamma genes.
A spontaneous mammary adenocarcinoma of BALB/c mice was transduced with the murine interleukin (IL)-2, IL-4, and interferon (IFN)-gamma genes. The ability of clones releasing IL-2, IL-4 or IFN-gamma to form tumors after s.c. challenge was compared to the TS/A parental cells (TS/A-pc) and to cells transduced with the neomycin resistance gene alone. Cytokine-gene-transduced clones activated a strong inflammatory reaction. The elicited by IL-2 and IL-4-gene-transduced cells efficiently led to tumor rejection. This reaction depended on the activation of several cell mechanisms, those classed as nonspecific being predominant. The repertoire of reactive leukocytes recruited in the reaction varies as a function of the secreted cytokine. The growth of a secondary contralateral TS/A-pc challenge after clone rejection was significantly impaired.