Cell invasion by Trypanosoma cruzi and the type I interferon response

Abstract

Invasion of nonphagocytic host cells and the concomitant activation of the innate immune response are among the earliest interactions between Trypanosoma cruzi and its mammalian host. During invasion of host cells, T. cruzi triggers diverse signaling pathways to subvert cellular processes. Here we discuss the evidence for three invasion routes that have been described as mechanistically distinct pathways in the past, as well as an emerging unified model which proposes they represent elements of the same overall invasion process. As a result of cell invasion, the innate immune response, specifically type I IFN production, is initiated in host cells. Although the signaling mechanisms leading to type I IFN production during T. cruzi infection remain poorly understood, this cytokine drives the global transcriptional profile of infected cells, influences the subsequent adaptative immune response and, under conditions of high parasite burden, is detrimental for the host. Here we discuss these early parasite/host interactions in the context of the establishment of intracellular infection by T. cruzi.