Human neutrophils and eosinophils adhere to the surface of schistosomula of Schistosoma mansoni that have been preincubated with antischistosomular sera with or without complement . Neutrophils are seen to form small (<0.5 Jim), heptalaminar and large (5-8 Am), pentalaminar fusions with the normal pentalaminar parasite surface membrane . By freeze-fracture techniques, attachment areas 5-8 Am in diameter are seen to form between neutrophils and schistosomula. These areas have three zones-an edge and two centrally located areas, one of which is rich and one of which is poor in intramembrane particles (IMPS) . The edge zone is continuous around the attachment areas and is usually composed of a skipfracture that passes out of the schistosomular outer membrane into the inner membrane . In some cases, the edge zone is made up of a string of IMPS . The IMP-rich central areas have an IMP concentration similar to that of unattached neutrophil membranes, are raised off of the surface of the schistosomulum, and have two normal schistosomular membranes underneath, indicating that they are indeed unattached . The IMP-poor central areas are composed of a fused or hybrid membrane that is continuous with the neutrophil plasma membrane but that bears the same spatial relationship to the schistosomular inner membrane that the normal outer membrane does . Similar changes are seen in samples prepared without glycerination. Eosinophils generally do not fuse with the schistosomular outer membrane but, instead, discharge their granular contents onto the surface of the schistosomula and appear to adhere to the parasite through this discharged material . It is suggested that schistosomula have a capability to fuse with mammalian cells and that this fusion proceeds from a fusion of the outer leaflets to a fusion of the bilayers, as appears also to be the case in other systems.Schistosoma mansoni presents a paradox in that adult parasites are able to survive in the bloodstream for long periods of time (years in some cases), whereas schistosomula, the larvae that develop from cercariae that have penetrated the skin, are destroyed by an antibody-dependent granulocyte reaction (31) . Two questions arise from this paradox. First, how do adult parasites avoid the immune response? One answer that has been given is that the parasites acquire host antigens, namely ABH blood group glycolipids (12), Forssman antigen (7), and components of the major histocompatibility complex (30), 46

Neutrophils and eosinophils adhering to the surface of schistosomula of Schistosoma mansoni have been partially or completely detached with hypertonic sucrose or by pipetting. The sucrose-treated neutrophils are attached only in areas where there are pentalaminar fusions between the neutrophil and tegumental membranes, suggesting that these fusions attach the cells to the parasites. Pipetting breaks many of the attached cells. In thin section, the tegumental membrane underlying these cells is seen to be pentalaminar. By freeze-fracture techniques, modified attachment areas are found. The edge zone often appears as a single strand of intramembrane particles (IMPs) on the P2 face and as a groove on the E2 face. The edge zone may also have large discontinuities, in which case it no longer separates membrane faces of unequal IMP density from one another. In addition, the IMPs on the IMP-rich areas become aggregated and surrounded by craters in the membrane. These experiments suggest that the fusions may be the mechanism by which the parasite acquires some host membrane components on its surface. On the other hand, eosinophil plasma membranes are seen adhering to a layer of electron-dense material on the parasite after the cells have been disrupted by pipetting. This suggests that eosinophils adhere to the parasite surface through their discharged granule material and not by membrane fusions.

Human buffy coat cells adhering to schistosomula of Schistosoma mansoni that were preincubated in fluorochrome-conjugated concanavalin A (Con A), wheat germ agglutinin, lentil lectin, or purified IgG from a hyperimmunized rabbit, were examined by fluorescence and transmission electron microscopy and by freeze-fracture. All four fluorochromeconjugated multivalent ligands were homogeneously distributed on the parasite surface after preincubation. Within 1-3 h after the addition of cells, large areas of nonfluorescence, 10-20 #m in diameter, were seen on the parasite surface. In addition, the fluorochromes were observed in granules within the cells. Electron microscope autoradiography of worms preincubated with 1251-Con A showed silver grains evenly distributed over the tegumental membrane. After the addition of cells, grains were seen over phagolysosomes in the cytoplasm of neutrophils adhering to the parasites. In addition, no grains were present over large areas of the tegumental membrane, which still retained its normal architecture, or over fusions between the neutrophil plasma membrane and the outer tegumental membrane. Rabbit IgG formed an electron-dense layer on the tegumental membrane which was endocytosed by neutrophils. Both neutrophils and eosinophils fused with the parasite in areas containing no electron-dense material on the surface. It is concluded that human neutrophils will endocytose a variety of multivalent ligands from the surface of schistosomula, which probably accounts for the failure of neutrophils to kill the parasite and acts to clear the parasite surface of both antigen and antibody. Presumably, the components of the parasite surface which have originally bound the ligands are also endocytosed since surface components labeled by galactose oxidase and NaBaH4 are taken into cells when examined by light microscope autoradiography. Finally, membrane fusion occurs in areas devoid of multivalent glands, which suggests that these ligands serve to bring the cells and parasites close together; but the actual fusigens probably reside in the lipids in the outer tegumental membrane.Schistosomula, larvae of Schistosoma mansoni, can be destroyed in vitro by human eosinophils--but not by neutrophils--after the parasites are preincubated in heat-inactivated sera from patients with schistosomiasis (28). Eosinophil-mediated killing is caused by exocytosis of lysosomes onto the parasite surface (3,7,17), and subsequent damage to the tegumental membrane is caused by major basic protein (2) and possibly peroxidases to which the worm is quite sensitive (13). The neutrophils, on the other hand, do not exocytose their lysosomes but instead fuse their plasma membranes with the outer tegumental membranes of the schistosomula over areas as large as 8 #m in diameter (3).In these experiments, we have promoted adherence between human buffy coat cells and schistosomula with three lectins concanavalin A (Con A), wheat germ agglutinin (WGA), and lentil lectin (Len), as well as with IgG purified from a hyperimmu...