Section of Surgical Oncology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792-7375, USA.
Cell Immunol. 2011;271(1):104-9. doi: 10.1016/j.cellimm.2011.06.011. Epub 2011 Jun 17.
We have observed that in vivo interaction between melanoma and resting T cells promotes suppression of antigen-driven proliferative T cell expansion. We hypothesized that this suppression would affect tumor antigen-specific T cell populations more potently than tumor-unrelated T cell populations. A B16F10 cell line was stably transfected to express low levels of the lymphocytic choriomeningitis virus (LCMV) glycoprotein GP33 (B16GP33). Mice bearing B16F10 or B16GP33 tumors were infected with LCMV, and proliferative expansion of LCMV epitope-specific T cell populations was quantified. In vitro and in vivo assays confirmed low levels of antigenic GP33 expression by B16GP33 tumors. Suppressed expansion of GP33-specific T cells was equivalent between mice bearing B16F10 and B16GP33 tumors. These observations suggest that the ability of growing melanoma tumors to impair antigen-driven proliferative expansion of activated T cells is global and not antigen-specific, and provide further insight into the influence of cancer on activated T cell homeostasis.
我们已经观察到,黑色素瘤与静息 T 细胞之间的体内相互作用会促进抗原驱动的增殖性 T 细胞扩增的抑制。我们假设这种抑制作用会比肿瘤无关的 T 细胞群体更有效地影响肿瘤抗原特异性 T 细胞群体。B16F10 细胞系被稳定转染以低水平表达淋巴细胞脉络丛脑膜炎病毒 (LCMV) 糖蛋白 GP33 (B16GP33)。携带 B16F10 或 B16GP33 肿瘤的小鼠感染 LCMV,并定量检测 LCMV 表位特异性 T 细胞群体的增殖扩增。体外和体内实验证实 B16GP33 肿瘤低水平表达抗原性 GP33。携带 B16F10 和 B16GP33 肿瘤的小鼠中,GP33 特异性 T 细胞的扩增受到抑制的程度相当。这些观察结果表明,生长中的黑色素瘤肿瘤抑制激活 T 细胞的抗原驱动性增殖扩增的能力是全球性的,而不是抗原特异性的,并进一步深入了解癌症对激活 T 细胞动态平衡的影响。