Mechanisms in the suppression of tumor rejection produced in mice by repeated UV irradiation.
Mechanisms in the suppression of tumor rejection produced in mice by repeated UV irradiation.
复制标题
反复紫外线照射抑制小鼠肿瘤排斥反应的机制。
作者：
S. Ullrich;M. Kripke
反复暴露在UVB(280到320 nm)辐射下的小鼠不能排斥高抗原性UVB诱导的皮肤癌，它们的淋巴器官含有T淋巴细胞，将这种能力转移到非免疫接受者。我们发现能够转移抑制肿瘤排斥反应的细胞的表型是Lyt-1+2-，Ia-。通过使用抗Lyt-1的单抗去除UVB照射小鼠的脾细胞的抑制活性，当注射到致死的x射线照射的受者体内时，产生了能够介导肿瘤排斥反应的细胞群。这一发现表明，UVB照射的小鼠不能排斥UVB辐射诱发的皮肤癌，这不是由于克隆缺失，例如，缺乏能够识别这些肿瘤上的抗原并对其做出反应的淋巴细胞，而可能仅仅取决于抑制淋巴细胞的活性。在一次UVB照射的小鼠未照射皮肤上涂抹恶唑酮诱导的抗原特异性抑制淋巴细胞表型为Lyt-1+2-，这一发现也与UVB诱导的两种免疫抑制机制相同的假设相一致。8-甲氧补骨脂素加UVA(320~400 nm)照射一次，然后用恶唑酮涂抹未暴露的皮肤，小鼠诱导的抑制细胞表型为Lyt-1+2+，这表明这种处理可能激活了不同的抑制途径。
Mice exposed repeatedly to UVB (280 to 320 nm) radiation are unable to reject highly antigenic UVB-induced skin cancers, and their lymphoid organs contain T lymphocytes that transfer this inability to nonimmune recipients. We show that the phenotype of the cells capable of transferring suppression of tumor rejection is Lyt-1+2-,Ia-. Removal of the suppressive activity of spleen cells from UVB-irradiated mice through the use of monoclonal anti-Lyt-1 antibodies resulted in a population of cells capable of mediating tumor rejection when injected into lethally x-irradiated recipients. This finding demonstrates that the inability of UVB-irradiated mice to reject skin cancers induced by UVB radiation is not due to clonal deletion, e.g., the absence of lymphocytes that are capable of recognizing and responding to antigens on these tumors, but instead is likely to depend solely on the activity of suppressor lymphocytes. The phenotype of antigen-specific suppressor lymphocytes induced by painting oxazalone on the unirradiated skin of mice exposed once to UVB radiation was Lyt-1+2-, also a finding consistent with the hypothesis that the two forms of UVB-induced immunosuppression occur by means of the same mechanism. The phenotype of suppressor cells induced in mice treated once with 8-methoxypsoralen plus UVA (320 to 400 nm) radiation, followed by painting unexposed skin with oxazalone, was Lyt-1+2+, suggesting that this treatment may activate a different suppressor pathway.