The mechanisms parasites have developed to escape immune surveillance are currently under investigation in many laboratories, because their elucidation may provide new approaches to the prevention of the diseases the parasites cause. For a detailed description and experimental evidence of these various mechanisms, see the recent review by Bloom (1).One possible means of evasion is the uptake of host antigen by the parasite (2). This phenomenon has been amply studied and documented in schistosomiasis. The acquisition of mouse antigens (3-5), human A, B, and H blood group antigens (6, 7), glycolipids from erythrocytes (8), serum factors (9-11) and, more recently, mouse histocompatibility antigens (12) have been demonstrated in this parasite and offer an effective mechanism for antigenic mimicry of the host and subsequent escape from the immune response.This same parasite has been used to study the possibility of immunological blockade (13). Host immunoglobulin has been shown to occur on the surface of Schistosoma mansoni (14,15), and it has also been determined that this immunoglobulin is heterospecific, excluding the possibility of a specific parasite-antigen host-antibody interaction (15). These studies also suggest that the host immunoglobulin adsorbed by the parasite is oriented so as to have a Fab region of the molecule available, possibly representing a specific binding of the immunoglobulin through a receptor for Fc present on the membrane of S. mansoni, Indeed, receptors for IgG Fc, human fl2-microglobulin (16), and Clq (17) on this parasite have recently been reported.