Cutaneous Leishmaniasis: The Complexity of Host’s Effective Immune Response against a Polymorphic Parasitic Disease

Figure 2

Inoculation of Leishmania promastigotes in the host dermis by the sand fly triggers the activation of the complement cascade. C3 convertase undergoes proteolytic cleavage, giving origin to the complement factors C3a and C5a. These chemotactic factors attract neutrophils (N) and macrophages (MΦ) to the infection site and induce the expression of the respective receptors. On the parasite membrane, the surface glycoprotein of 63 kDa (gp63) can convert C3b to the inactive form (C3bi), which avoids the assembly of the lytic complex (MAC) on the parasite surface. In turn, C3bi binds to the MΦ receptor (RC3), promoting fast parasite phagocytosis.