Cell surface receptor that binds to human complement C2a protein. This results in inhibition of the classical and lectin pathways of complement activation, probably due to interference with binding of C2a to C4b and interference with cleavage by C1 or MASP2 such that C3 convertase cannot be formed. This infers resistance to complement-mediated cell lysis, allowing parasite survival and infection. Interacts (via N-terminal extracellular domain) with human C2a. Located on the surface tegumental plasma membrane of metacyclic trypomastigote so in contact with host blood plasma. In Y strain, expression is seen in metacyclic trypomastigote form and in stationary, but not logarithmic-phase epimastigote forms. In Colombiana strain, expression is seen in metacyclic trypomastigote form only. The C-sensitive epimastigote form of the Colombiana strain is more susceptible to lysis than the Y strain at all human serum concentrations. Potential vaccine candidate molecule.