The Dialogue of the Host-Parasite Relationship: Leishmania spp. and Trypanosoma cruzi Infection

Figure 1

Leishmania survival and host cell modulation: The LPG coating of the parasites prevents the complement membrane attack complex insertion. In addition, the promastigote kinase phosphorylates the components of the complement, inhibiting its activation. Promastigote opsonized by C3bi interacts with macrophage membrane CR3 activating tyrosine phosphatase that dephosphorylates STAT-1 leading to inhibition of transcription of the IL-12p40 gene. During the process of promastigote internalization LPG is transferred from parasite membrane to host cell membrane promoting lipid microdomain disruption inhibiting PKC activation and ROS generation (burst oxidative). Inside the parasitophorous vacuole (PV) membrane, this disruption causes the exclusion of synaptotagmins V (Syt V), abrogating the recruitment of the vacuolar ATPase and, consequently, PV acidification allowing the survival of promastigotes. The Leishmania dsRNA virus (LRV1) binds toll-like receptor 3 (TLR3) triggering strong IFN-β production and downregulation of IFNγ-R. Already gp63 cleaves SHP1 prevents classical macrophage activation by IFN-γ. N—nucleus, PV—parasitophorous vacuole and V—vacuole.