A 'devil' of a problem

Abstract

The discovery of a second facial tumor disease in the Tasmanian devil has provided insights into the emergence of contagious cancers.

Keywords: MHC; MHC-1; Sarcophilus harrisii; Tasmanian devil; cancer biology; contagious cancer; immune escape; immunology; inflammation.

Figure 1.. Schematic illustrating the mechanisms underlying devil facial tumor disease.

The immune system identifies cells that should not be in an organism based on foreign or abnormal peptides (grey triangles) presented in the binding groove of MHC-I molecules on the surface of the cell. DFT1 cells (top) avoid the immune system of the Tasmanian devil by losing expression of their MHC-I molecules (orange and blue). DFT2 cells (bottom left) appear to be developing a similar trick, but still express a number of MHC-I molecules (shown in black) that can be recognized by the immune system. However, Caldwell et al. found that DFT2 cells are starting to lose MHC-I molecules (bottom right), which suggests that this form of tumor could soon become as pathogenic as DFT1. DFT1 and DFT2 also appear to share gene alleles of MHC-I genes (orange and blue), suggesting there may be something about these variants associated with the emergence of a contagious tumor.