Escape from the action of Ab

T. cruzi can limit the Fc-dependent effector functions of specific Ab bound to its surface by two mechanisms. First, cruzipain can digest the Fc part of IgG, impairing their binding to FcR.²⁰³ Second, it expresses on its surface a factor that binds mammalian Igs through their Fc fragment,²⁰⁴ inhibiting Ig-mediated attachment and penetration of T. cruzi into macrophages.

T. cruzi TS also contributes to parasite survival. During the acute phase, TS molecules bearing SAPA repeats are abundantly released by the parasite. The immunodominance of SAPA prevents the early formation of neutralizing Ab directed against the catalytic site, situated away on the molecule. As long as TS enzyme is active, it profits the parasite by favoring host cell invasion²⁰⁵ and conferring resistance to lytic anti-a-GAL Ab.⁶ Later on, when SAPA sequences are masked by Abs, TS-neutralizing Ab are produced. Neutralization of TS activity favors survival of the host by limiting massive cell invasion by the parasite.²⁰⁵