Chagas disease: the peculiar relationship between parasite and host.

Clinical course of Chagas disease (CD), caused by the protozoan parasite Trypanosoma cruzi, usually progresses from an acute to an indeterminate phase, both characterized by the lack of specific symptoms. Only one third of patients develop life-threatening manifestations associated with the chronic infection. This fact draws attention of the scientific community to understanding the role of the immune response in the course of the disease, which is the aim of this review. On the one hand, both innate and adaptive immune cells exert antiparasitic effects by respectively releasing nitric oxide and antibodies, as well as activating perforin/granzyme or Fas/FasL pathways. Moreover, nature of secreted cytokines (i.e., pro- or anti-inflammatory) polarizes the response towards Th1 or Th2: according to the phase of CD, these profiles can be detrimental or beneficial to the host. On the other hand, the parasite has developed strategies to escape from the immune system and successfully establish the chronic disease. Also, parasite persistence, together with the immunopathology generated by the infection, seems to be important for the onset of such symptomatic phase. Since the immune response evolves through CD progression and has close relationship with the severity of the disease, study of immune mediators deserves special attention, to identify intervention points for preventing CD evolution and developing more effective therapies.