There is a general
consensus that during chronic
Trypanosoma cruzi infection, the host
immune system induces complex processes to ensure the control of
parasite growth while preserving the potential to mount and maintain a
life-long controlled humoral and
cellular immune response against the invading pathogen. This
review summarises evidence in an attempt to elucidate "what must be understood" to further clarify the
role of
innate immunity in the development/
maintenance of clinical
Chagas disease and the impact of etiological
treatment on host
immunity, highlighting the contributions of the
innate immunity and regulatory T (Treg)
cells. Recently, increasing focus on
innate immunity suggest that chronic T. cruzi
infection may cause
morbidity when innate effector functions, or the
down-regulation of adaptive regulatory mechanisms are lacking. In this context, stable asymptomatic
host-parasite interactions seem to be influenced by the effector/regulatory balance with the participation of
macrophages, natural killer (NK) and CD8+
T cells in parallel with the establishment of regulatory mechanisms mediated by NKT and
Treg cells. Moreover, a balanced innate immune activation
state, apart from
Treg cells, may
play a
role in controlling the adverse events triggered by the massive
antigen release induced by
trypanosomicidal agents during
Chagas disease etiological
treatment.