David Quammen Harper’s magazine

The biological mystery of how the Tasmanian devil’s rogue tumor manages to establish itself in one animal after another is still unsolved. But a good hypothesis has been offered by an immunologist named Greg Woods at the University of Tasmania. Woods and his group studied immune reactions in Sarcophilus harrisii, which seem generally to be normal against ordinary sorts of infection. Against DFTD cells, though, no such reaction occurs. “The tumor is just not seen by the immune system, because it just looks too similar,” Woods told me when I stopped by his lab. The devils have low genetic diversity, probably because they inhabit a small island, they colonized it originally by way of just a few founders, and they have passed through some tight population bottlenecks in the centuries since. They’re not quite so alike one another as a bunch of inbred hamsters, but they’re too alike for their own good in the current sad, anomalous circumstances. Their immune systems don’t reject the tumor cells because, Woods suspects, in each animal the critical MHC genes (the major histocompatibility complex, which produces proteins crucial to immunological policing) are all virtually identical, and the devils’ police cells can’t distinguish “him” from “me.” Read more here