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 (By similarity). Interacts (via N-terminal extracellular domain) with human C2a. Highly expressed in parasitic larvae (cercariae). Phosphorylated on tyrosine residues. Potential vaccine candidate molecule.