Berendt M J, North R J
J Exp Med. 1980 Jan 1;151(1):69-80. doi: 10.1084/jem.151.1.69.
The results of this paper are consistent with the hypothesis that progressive growth of the Meth A fibrosarcoma evokes the generation of a T-cell-mediated mechanism of immunosuppression that prevents this highly immunogenic tumor from being rejected by its immunocompetent host. It was shown that it is possible to cause the regression of large, established Meth A tumors by intravenous infusion of tumor-sensitized T cells from immune donors, but only if the tumors are growing in T-cell-deficient recipients. It was also shown that the adoptive T-cell-mediated regression of tumors in such recipients can be prevented by prior infusion of splenic T cells from T-cell-intact, tumor-bearing donors. The results leave little doubt that the presence of suppressor T cells in T-cell-intact, tumor-bearing mice is responsible for the loss of an earlier generated state of concomitant immunity, and for the inability of intravenously infused, sensitized T cells to cause tumor regression. Because the presence of suppressor T cells generated in response to the Meth A did not suppress the capacity of Meth A-bearing mice to generate and express immunity against a tumor allograft, it is obvious that they were not in a state of generalized immunosuppression.
Meth A纤维肉瘤的渐进性生长引发了一种T细胞介导的免疫抑制机制,该机制可防止这种高免疫原性肿瘤被其具有免疫活性的宿主排斥。研究表明,通过静脉输注来自免疫供体的肿瘤致敏T细胞,可以使已形成的大型Meth A肿瘤消退,但前提是肿瘤在T细胞缺陷的受体中生长。研究还表明,在此类受体中,通过预先输注来自未切除肿瘤的T细胞完整供体的脾T细胞,可以防止过继性T细胞介导的肿瘤消退。结果毫无疑问地表明,未切除肿瘤的T细胞完整小鼠中抑制性T细胞的存在,是导致早期产生的伴随免疫状态丧失的原因,也是静脉输注的致敏T细胞无法引起肿瘤消退的原因。由于响应Meth A产生的抑制性T细胞的存在并未抑制携带Meth A的小鼠产生和表达针对肿瘤同种异体移植物的免疫的能力,显然它们并非处于全身性免疫抑制状态。