Trypanosoma cruzi parasites fight for control of the JAK-STAT pathway by disarming their host.

The zoonotic Chagas' disease is caused by infections with the hemoflagellate Trypanosoma cruzi (T. cruzi) which is endemic in Latin America. Despite recent advances in our understanding of the pathogenesis of the disease, the underlying molecular processes involved in host-parasite interactions are only poorly understood. In particular, the mechanisms for parasite persistence in host cells remain largely unknown. Cytokine-driven transcription factors from the family of STAT (signal transducer and activator of transcription) proteins appear to play a central role in the fight against T. cruzi infection. However, amastigotes proliferating in the cytoplasm of infected host cells develop effective strategies to circumvent the attack executed by STAT proteins. This review highlights the interactions between T. cruzi parasites and human host cells in terms of cytokine signaling and, in particular, discusses the impact of STATs on the balance between parasite invasion and clearance.