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首页> 外文期刊>Oncogene >Antigen-specific immunity does not mediate acute regression of UVB-induced p53-mutant clones
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Antigen-specific immunity does not mediate acute regression of UVB-induced p53-mutant clones

机译：抗原特异性免疫不能介导UVB诱导的p53突变克隆的急性退化

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Chronic irradiation of human or murine epidermis with ultraviolet B (UVB) induces clones of p53-mutant keratinocytes. Clones precede and parallel the induction of carcinomas, suggesting that they are an early stage of UVB carcinogenesis. In the absence of UVB, these clones rapidly regress. For UVB-induced murine skin tumors and papillomas, regression is known to involve antigen-specific immunity. To determine whether antigen-specific immunity influences the creation, expansion, or regression of p53-mutant clones, we studied Rag1 knockout mice deficient in the recombination activating gene 1 required for development of B, T, T, and natural killer T cells. Since tissue homeostasis could affect proliferation or persistence of clones, we also examined the effect of Rag1 on UVB-induced hyperplasia and apoptosis. Mice were irradiated with UVB daily for 7–11 weeks to create p53-mutant clones, and then retained in the absence of UV. After UV ended, epidermal thickness decreased and p53-mutant clones observed in the epidermal sheets regressed, with no significant differences between Rag1-/- and wild type. During the initial chronic UVB irradiation, increasing irradiation time increased both the number and size of p53-mutant clones, with no significant difference between genotypes. We conclude that antigen-specific immunity is not involved in the initiation, expansion, or acute regression of p53-mutant clones.
机译：用紫外线B（UVB）长期照射人或鼠的表皮会诱导p53突变的角质形成细胞克隆。克隆先于癌症并与之平行，这表明它们是UVB癌变的早期阶段。在没有UVB的情况下，这些克隆会快速消退。对于UVB诱导的鼠类皮肤肿瘤和乳头状瘤，已知消退涉及抗原特异性免疫。为了确定抗原特异性免疫是否影响p53突变克隆的产生，扩增或消退，我们研究了缺乏Rag1基因敲除小鼠，该小鼠缺乏B，T，T和自然杀伤性T细胞发育所需的重组激活基因1。由于组织稳态可能会影响克隆的增殖或持久性，因此我们还研究了Rag1对UVB诱导的增生和凋亡的影响。每天用UVB照射小鼠7-11周以产生p53突变克隆，然后在不存在UV的情况下保留。 UV结束后，表皮厚度减少，在表皮片中观察到的p53突变克隆消退，Rag1-/-和野生型之间无显着差异。在最初的慢性UVB照射过程中，增加照射时间会增加p53突变体克隆的数量和大小，而基因型之间无显着差异。我们得出结论，p53突变克隆的起始，扩增或急性消退不涉及抗原特异性免疫。

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