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重复紫外线照射对小鼠肿瘤排斥反应抑制作用的机制。

Mechanisms in the suppression of tumor rejection produced in mice by repeated UV irradiation.

作者信息

Ullrich S E, Kripke M L

出版信息

J Immunol. 1984 Nov;133(5):2786-90.

PMID:6237155
Abstract

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.

摘要

反复暴露于UVB(280至320纳米)辐射的小鼠无法排斥高抗原性UVB诱导的皮肤癌,并且它们的淋巴器官含有能将这种无能力转移给非免疫受体的T淋巴细胞。我们发现,能够转移肿瘤排斥抑制作用的细胞表型为Lyt-1+2-、Ia-。通过使用单克隆抗Lyt-1抗体去除UVB照射小鼠脾细胞的抑制活性,得到一群细胞,当将其注射到经致死性X射线照射的受体中时,能够介导肿瘤排斥。这一发现表明,UVB照射小鼠无法排斥UVB辐射诱导的皮肤癌并非由于克隆缺失,例如不存在能够识别这些肿瘤上的抗原并对其作出反应的淋巴细胞,而是可能仅取决于抑制性淋巴细胞的活性。通过在一次暴露于UVB辐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性淋巴细胞的表型也是Lyt-1+2-,这一发现也与两种形式的UVB诱导的免疫抑制通过相同机制发生的假设一致。在用8-甲氧基补骨脂素加UVA(320至400纳米)辐射处理一次,然后在未暴露皮肤上涂抹恶唑酮的小鼠中诱导的抑制细胞的表型为Lyt-1+2+,这表明这种处理可能激活了不同的抑制途径。

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