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首页> 外文期刊>The Journal of investigative dermatology. >IL-12 and IL-23 affect photocarcinogenesis differently
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IL-12 and IL-23 affect photocarcinogenesis differently

机译：IL-12和IL-23对光致癌作用的影响不同

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Induction of DNA damage by UVR is the key event in photocarcinogenesis. IL-12 and IL-23 are related heterodimeric cytokines consisting of a common p40 unit and a p35/IL-12 and a p19/IL-23 chain, respectively. Both exert immunomodulatory activities but are also found to reduce UVR-induced DNA damage presumably via induction of DNA repair. As both cytokines are also produced in the skin, they may mitigate the risk to develop UVR-induced skin cancer. This appears to be the case as mice lacking p40 were previously shown to be at higher risk for skin tumors upon chronic UVR exposure. As these mice express neither IL-12 nor IL-23, the individual effects of IL-12 or IL-23 could not be evaluated. Thus, mice lacking p35 (IL-12p35-/-) or p19 (IL-23p19-/-) were subjected to chronic UVR exposure. The Kaplan-Meier analysis indicated a significantly increased probability of tumor development in IL-23p19-/-but not in IL-12p35-/-mice. Taken together, in our model, loss of IL-23, but not of IL-12, enhances development of UVR-induced skin tumors, indicating that IL-23 but not IL-12 may counteract photocarcinogenesis. This may have impact on the development of future strategies utilizing antibodies against IL-12 and IL-23, respectively, for the treatment of inflammatory dermatoses.
机译：UVR诱导DNA损伤是光致癌作用中的关键事件。 IL-12和IL-23是相关的异二聚体细胞因子，分别由一条共同的p40单元和一条p35 / IL-12和一条p19 / IL-23链组成。两者均发挥免疫调节活性，但也可能通过诱导DNA修复来减少UVR诱导的DNA损伤。由于两种细胞因子也都在皮肤中产生，因此它们可以减轻发生UVR诱导的皮肤癌的风险。这似乎是事实，因为先前已证明缺乏p40的小鼠在长期UVR暴露下有较高的皮肤肿瘤风险。由于这些小鼠既不表达IL-12也不表达IL-23，因此无法评估IL-12或IL-23的个体作用。因此，缺乏p35（IL-12p35-/-）或p19（IL-23p19-/-）的小鼠受到慢性UVR照射。 Kaplan-Meier分析表明在IL-23p19-/-小鼠中肿瘤发展的可能性显着增加，但在IL-12p35-/-小鼠中却没有。两者合计，在我们的模型中，IL-23而非IL-12的丢失增强了UVR诱导的皮肤肿瘤的发展，表明IL-23而非IL-12可能抵消光致癌作用。这可能会影响分别使用针对IL-12和IL-23的抗体治疗炎症性皮肤病的未来策略的开发。

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