IL-12 is known primarily for its crucial role in the immune system. Now we have evidence that it can also enhance DNA repair in response to UVB. Schwarz and colleagues examined keratinocytes exposed to UVB in vitro and found that IL-12 can reduce apoptosis and improve their survival. This effect only applies to UVB, as IL-12 gives no resistance to γ-irradiation. Moreover, when mice themselves were exposed to radiation, IL-12 knockout mice produced greater numbers of sunburn cells than did wild-type mice, a phenotype that is partially restored by subcutaneous injection of IL-12 .
The authors report that treatment with IL-12, both in vitro and in vivo, is associated with a reduction in pyrimidine dimers, the predominant form of UVB-induced DNA damage. No reduction is seen 10 minutes after UVB irradiation, but is apparent 3.5 hours later, implying that IL-12 is having an effect following the initial insult. A mechanistic explanation is suggested by their observation that IL-12 treatment enhances NER and is associated with increased expression of NER-associated genes. As further confirmation of this hypothesis, IL-12 affords no protection to Xpa knockout mice, which lack a component of the NER system.
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