Inadequate epidermal homing leads to tissue damage in human cutaneous leishmaniasis.

Leishmaniasis is a model disease for the study of immunoregulatory mechanisms associated with host resistance and susceptibility. In this article, Felix Tapia and colleagues propose that defects in the signaling properties of the epidermis can result in the generation of either a chronic granulomatous response, which is unable to eliminate the parasite, or a proinflammatory mucocutaneous response and tissue damage.