Although a murine contact hypersensitivity model is useful to elucidate some aspects of ACD pathogenesis, the murine model is different from ACD in humans due to the following: (1) functions and population densities of specific immune cell types (Th22 cells; γδT cells) are different; (2) surface markers for each immune cell type are not always identical (CD1a for human LCs); and (3) weak sensitizers (nickel) which are usually sufficient to cause ACD in patients cannot induce reactions in mice. Here, CD1A is linked to granular corneal dystrophy type II.