Published online 17 December 2001. doi:10.1083/jcb1557rr3
© The Rockefeller University Press,
0021-9525/2001/12/1094-b $5.00
The Journal of Cell Biology, Volume 155, Number 7, December 24, 2001 1094-b-1094
Repair long and prosper
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DNA damage (brown, top) is reduced by IL-12 (bottom).
Schwarz/Macmillan
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Death can be a good thing when it comes to sunburn—the death of UVB-damaged cells reduces the chances of cancerous growths arising. But now, Thomas Schwarz (University of Münster, Münster, Germany) and colleagues have found a way that the body can reduce the evil effects of UVB without invoking death. A cytokine, IL-12, induces nucleotide excision repair (NER), and thus decreases DNA damage and apoptosis.Schwarz started out by looking for factors that enhanced apoptosis after UV treatment. Instead, he found the reverse effect with IL-12. A series of follow-up studies failed to demonstrate an underlying mechanism. "At the very end, more in desperation, we checked DNA damage," he says. The finding of reduced DNA damage was a surprise, as cytokines have not previously been implicated in inducing NER. IL-12's protective effect seems to be dependent on NER induction, as the improvement was lost in a mouse that had a mutation in the NER system.
Could IL-12 eliminate flaking skin from summer holidays? "It's tempting to speculate on the prophylactic uses," says Schwarz. "But I don't claim that applying IL-12 will be the protective strategy of tomorrow," especially as such a treatment could increase the chances of autoimmunity. Schwarz suggests, however, that a better understanding of this pathway may help improve sunscreens. 
Reference:
Schwarz, A., et al. 2001. Nat. Cell Biol. 10.1038/ncb717.
William A. Wells
wellsw{at}rockefeller.edu
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