Schistosomes put the stoppers on Langerhans cell migration

Abstract

Trottein and colleagues have proposed a new mechanism by which schistosomes can evade the host immune system [Angeli, V. et al. (2001) J. Exp. Med. 193, 1135–1148]. Their study focused on the interactions between parasites and the skin's immune surveillance cells, Langerhans cells (LCs). LCs are normally responsible for engulfing pathogen-derived antigens in the skin and trafficking to the lymph nodes to activate antigen-specific T cells. Using a murine model of percutaneous schistosomiasis, the authors found that the LCs were prevented from normal skin-exiting behavior. Instead, the LCs were retained in the infected epidermis and were not able to activate T cells in the lymph node. The inhibitory effect of schistosomes on LC migration was found to be mediated by the action of parasite-derived prostaglandin D2 (PGD2) and not by host factors. PGD2 might play a hitherto unrecognized key role in the regulation of cutaneous immune responses. SHK