Antonia S J, Muñoz-Antonia T, Soldevila G, Miller J, Flavell R A
Section of Immunobiology, Yale School of Medicine, New Haven, Connecticut 06510, USA.
Cancer Res. 1995 Jun 1;55(11):2253-6.
The existence of a naturally occurring immunosurveillance against neoplastic cells is controversial. A difficulty with this concept is that tumor-specific antigen-reactive T cells would not be expected to become activated after encountering tumor cells, since T cells that bind to antigen in the absence of the costimulation provided by antigen-presenting cells may be inactivated. We studied a transgenic model of tumorigenesis where T cells reactive to a particular tumor-specific antigen are lost prior to the development of non-antigen-presenting cell-derived tumors; therefore, the tumors that develop are not subjected to immunosurveillance. We found that a tumor cell line derived from one such tumor expresses the T-cell costimulatory molecule B7-1, the expression of which is normally restricted to antigen-presenting cells. In addition, we found that several immortalized cell lines, which are nontumorigenic and thus have suffered only early genetic events in the tumorigenesis process, express B7. This suggests that a host cell can be induced to express surface B7-1 molecules after suffering an oncogenic insult, which might possibly be a primary mechanism of immunosurveillance against tumors.
针对肿瘤细胞的天然免疫监视的存在存在争议。这一概念的一个难点在于，肿瘤特异性抗原反应性T细胞在遇到肿瘤细胞后预计不会被激活，因为在没有抗原呈递细胞提供的共刺激的情况下与抗原结合的T细胞可能会失活。我们研究了一种肿瘤发生的转基因模型，其中对特定肿瘤特异性抗原具有反应性的T细胞在非抗原呈递细胞衍生的肿瘤发生之前就已丧失；因此，所形成的肿瘤不受免疫监视。我们发现，源自其中一种此类肿瘤的肿瘤细胞系表达T细胞共刺激分子B7-1，其表达通常仅限于抗原呈递细胞。此外，我们发现几种永生化细胞系，它们不具有致瘤性，因此在肿瘤发生过程中仅经历了早期遗传事件，也表达B7。这表明宿主细胞在遭受致癌损伤后可被诱导表达表面B7-1分子，这可能是针对肿瘤的免疫监视的主要机制。
