Musiani P, Modesti A, Brunetti M, Modica A, Vitullo P, Gulino A, Bosco M C, Colombo M P, Nanni P, Cavallo F
Institute of Experimental Pathology and Social Medicine, University of Chieti, Italy.
Nat Immun. 1994 Mar-Jun;13(2-3):93-101.
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.
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。将分泌IL-2、IL-4或IFN-γ的克隆在皮下攻击后形成肿瘤的能力与TS/A亲本细胞(TS/A-pc)以及仅用新霉素抗性基因转导的细胞进行比较。细胞因子基因转导的克隆激活了强烈的炎症反应。IL-2和IL-4基因转导的细胞引发的反应有效地导致了肿瘤排斥。这种反应依赖于几种细胞机制的激活,其中非特异性机制占主导。反应中募集的反应性白细胞库随分泌的细胞因子而变化。克隆排斥后对侧二次TS/A-pc攻击的生长明显受损。