Waldner C I, Mongini C, Alvarez E, Sánchez Lockhart M, Gravisaco M J, Hajos S E
Cátedra de Immunologia, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, IDEHU, Argentina.
Br J Cancer. 1997;75(7):946-50. doi: 10.1038/bjc.1997.165.
As it has been suggested that an autocrine mechanism may control tumour cell growth, in this work cells from a spontaneous murine T lymphocyte leukaemia (LB) expressing the interleukin-2 receptor (IL-2R) (CD25) were evaluated in vitro for IL-2-mediated autocrine growth. Cells grew readily in culture and proliferation was enhanced by the addition of recombinant IL-2 but inhibited by monoclonal antibodies against either IL-2 or IL-2 receptor, in the absence of exogenous IL-2. Cyclosporin A also inhibited LB cell growth. However, when exogenous IL-2 was added together with cyclosporin A, cell proliferation proved similar to controls. Using reverse transcription polymerase chain reaction (PCR), mRNA for IL-2 was found to be present in tumour cells. Our findings support the hypothesis that LB tumour cell proliferation is mediated by an autocrine pathway involving endogenous IL-2 generation, despite the fact that these cells are not dependent on exogenous IL-2 to grow in culture.
由于有人提出自分泌机制可能控制肿瘤细胞生长,在本研究中,对来自表达白细胞介素-2受体(IL-2R)(CD25)的自发性小鼠T淋巴细胞白血病(LB)的细胞进行了体外IL-2介导的自分泌生长评估。细胞在培养中易于生长,添加重组IL-2可增强增殖,但在无外源性IL-2的情况下,抗IL-2或IL-2受体的单克隆抗体可抑制增殖。环孢素A也抑制LB细胞生长。然而,当外源性IL-2与环孢素A一起添加时,细胞增殖与对照组相似。使用逆转录聚合酶链反应(PCR),发现肿瘤细胞中存在IL-2的mRNA。我们的发现支持这样的假设,即LB肿瘤细胞增殖是由涉及内源性IL-2产生的自分泌途径介导的,尽管这些细胞在培养中生长不依赖外源性IL-2。