Trypanosoma cruzi Evades the Complement System as an Efficient Strategy to Survive in the Mammalian Host: The Specific Roles of Host/Parasite Molecules and Trypanosoma cruzi Calreticulin.

摘要: American Trypanosomiasis is an important neglected reemerging tropical parasitism, infecting about 8 million people worldwide. Its agent, Trypanosoma cruzi, exhibits multiple mechanisms to evade the host immune response and infect cells. An evasion strategy of T. cruzi infective stages its capacity inhibit complement system activation on parasite surface, avoiding opsonizing, stimulating lytic effects. Epimastigotes, non-infective form parasite, present in triatomine arthropod vectors, are highly susceptible complement-mediated lysis while trypomastigotes, form, bloodstream, resistant. Thus susceptibility varies depending stage (amastigote, trypomastigotes or epimastigote) strain. To avoid lysis, express surface a variety regulatory proteins, such as glycoprotein 58/68 (gp58/68), protein (TcCRP), trypomastigote decay-accelerating factor (T-DAF), C2 receptor inhibitor trispanning (CRIT) calreticulin (TcCRT). Alternatively, concomitantly, captures components with activity from H (FH) plasma membrane-derived vesicles (PMVs). All these proteins different steps classical (CP), alternative (AP) lectin pathways (LP). Thus, TcCRP inhibits CP C3 convertase assembling, gp58/68 AP convertase, T-DAF interferes convertases TcCRT LP, CRIT confers ability resist FH used by PMVs LP convertases. Many have similar molecular inhibitory mechanisms. Our laboratory has contributed elucidate role host-parasite interplay. we proposed that pleiotropic molecule, not only endoplasmic reticulum, but also participating key processes establish infection, inhibition serving virulence factor. Additionally, interaction components, participates anti-angiogenic anti-tumor inhibiting at least part, tumor growth infected animals.