Interferon gamma induces lung colonization by intravenously inoculated B16 melanoma cells in parallel with enhanced expression of class I major histocompatibility complex antigens.
Interferon gamma induces lung colonization by intravenously inoculated B16 melanoma cells in parallel with enhanced expression of class I major histocompatibility complex antigens.
复制标题
DOI：
10.1073/pnas.84.10.3405
复制
发表时间：
1987-05
影响因子：
11.1
通讯作者：
K. Taniguchi;M. Petersson;P. Höglund;R. Kiessling;G. Klein;K. Kärre
中科院分区：
文献类型：
--
作者：
K. Taniguchi;M. Petersson;P. Höglund;R. Kiessling;G. Klein;K. Kärre
用生理剂量的干扰素-γ（IFN-γ）治疗H-2缺陷的非转移性B16黑色素瘤细胞在体外降低了细胞生长，但在静脉注射经处理的细胞后评估，诱导了向肺定殖表型的转变。在每只注射的小鼠中，每毫升1抗病毒单位的重组IFN-γ诱导B16细胞形成3-40个肺转移，而需要1000倍更高浓度的IFN-β才能看到类似的效果。IFN-γ可以诱导有助于肿瘤细胞转移能力的细胞表面分子。IFN-γ处理B16细胞后转移能力的有效增强被H-2抗原表达的增加和对自然杀伤细胞的敏感性的降低所抵消。这些实验支持这样的观点，即转移可能不仅仅取决于肿瘤群体内稳定的遗传变化或异质性，还可能通过生理或药理学试剂对表型的调节而受到影响。结果还讨论了不同的效应细胞在肿瘤细胞清除中的作用，并与淋巴因子为基础的治疗策略。
Treatment of H-2-deficient nonmetastatic B16 melanoma cells with physiological doses of interferon gamma (IFN-gamma) reduced cellular growth in vitro but induced a shift to the lung-colonizing phenotype as assessed after intravenous injection of the treated cells. As little as 1 antiviral unit of recombinant IFN-gamma per ml induced B16 cells to form 3-40 pulmonary metastases in each injected mouse, whereas a 1000-fold higher concentration of IFN-beta was required to see similar effects. IFN-gamma may induce cell-surface molecules that contribute to the metastatic ability of the tumor cells. The efficient enhancement of metastatic ability after IFN-gamma treatment of the B16 cells was paralleled by an increased H-2 antigen expression and decreased sensitivity to natural killer cells. The experiments support the idea that metastasis may not depend exclusively on stable genetic changes or heterogeneity within a tumor population but may be also influenced through the modulation of the phenotype by physiological or pharmacological agents. The results are also discussed with regard to the role of different effector cells in tumor cell clearance and in relation to lymphokine-based strategies for therapy.