Abstract
Chagas disease is caused by the protozoan parasite Trypanosoma cruzi and is an important endemic infection in Latin America. Lately, it has also become a health concern in the United States and Europe. Most of the immunomodulatory mechanisms associated with this parasitic infection have been attributed to mucin-like molecules on the T. cruzi surface. Mucins are high molecular weight glycoproteins that are involved in regulating diverse cellular activities in both normal and pathological conditions. In Trypanosoma cruzi infection, the parasite-derived mucins are the main acceptors of sialic acid and it has been suggested that they play a role in various host-parasite interactions during the course of Chagas disease. Recently, we have presented evidence that sialylation of the mucins is required for the inhibitory effects on CD4(+) T cells. In what follows we propose that signaling via sialic acid-binding Ig-like lectin receptors for these highly sialylated structures on host cells contributes to the arrest of cell cycle progression in the G1 phase and may allow the parasite to modulate the immune system of the host.