Capping of Immune Complexes by Sporozoites of Eimeria tenella

Abstract

Sporozoites of Eimeria tenella were incubated for 10, 20, or 30 min with parasite-specific monoclonal IgG antibody 3D3II from mice and then rinsed in a Tris-buffered glucose saline solution (TBGS). Some sporozoites were then incubated for 10, 20, or 30 min with ferritin- or colloidal gold-conjugated goat anti-mouse IgG antibody and then fixed in 2.5% glutaraldehyde and prepared for transmission (TEM) or scanning (SEM) electron microscopy. Other sporozoites that had been previously exposed to monoclonal antibody were prefixed with 0.25% glutaraldehyde, incubated with ferritin- or colloidal gold-conjugated anti-mouse IgG antibody and then fixed and prepared for TEM or SEM. Control preparations consisted of sporozoites exposed only to TBGS, monoclonal antibody 3D3II or to ferritin- or colloidal gold-conjugated anti-mouse IgG antibody. Capping of immune complexes occurred only on the surface of those sporozoites exposed to monoclonal antibody 3D3II followed by ferritin- or gold-conjugated antibody. Immune complexes moved laterally and posteriorly on the outer surface of the parasite plasma membrane to form a cap at the posterior end of the sporozoite. Capping did not occur in TBGS controls nor in sporozoites treated with monoclonal antibody 3D3II and prefixed in 0.25% glutaraldehyde before exposure to ferritin- or gold-conjugated antibody. Thus, capping of surface antigens did not occur in the presence of monoclonal 3D3II antibody only, whereas specimens exposed to both monoclonal and ferritin- or colloidal gold-conjugated antibodies were able to cap immune complexes.

Coccidia: A review of recent advances on immunity and vaccine development

“…Inhibition may involve specific antibodies in the mucosa of immune birds which act by directly blocking invasion or by enhancing intraluminal destruction of sporozoites. However, E. tenella has been observed capping and shedding immune complexes (Speer et al, 1985b), and sporozoites taken from the caeca of immune birds develop normally when transferred to naive chickens (Rose, 1987). Conversely, E. acervulina immune birds had 11% more intracellular sporozoites (Augustine & Danforth, 1986) than controls, but they do not develop indicating that immunity interferes with further development, not simply invasion.…”

Ultrastructural localization of IgA and IgG receptors on oocysts, sporocysts, sporozoites, and merozoites of Eimeria falciformis

“…As suggested by Davis and Porter (1979), antibodies or enzymes within digestive tracts of immune animals may not completely abolish host cell penetration, but may alter parasites rendering them incapable of further development. Speer et al (1985) found that jncubation in a monoclonal antibody alone did not by itself induce capping of immune complexes by E . tenella sporozoites.…”

“…Except for the work of Speer et al (1983aSpeer et al ( , 1983Speer et al ( b, 1985 concerning monoclonal antibodies, there have been no previous immunoelectron microscopy (IEM) investigations using imrnunodeterminate site markers on Eimeria species. We report herein the ultrastructural localization of parasite-specific IgA and IgG on Eimeria falciformis oocysts, sporocysts, sporozoites , and merozoites.…”

Tegumental surface modulation in Schistosoma mansoni primary sporocysts in response to ligand binding

“…It is unclear as to the precise fate of ligands cleared from the surface of sporocysts. Mammalian lymphocytes and fibroblasts predominantly endocytose 'capped' complexes (Raff & de Petris 1973, Bretscher 1984, while most parasitic protozoans shed surface immune complexes (Dzbenski et a1 1976, Schmunis et al 1980, Speer et al 1985. Samuelson, Caulfield & David (1981) documented lateral mobility and shedding of con A-receptor complexes with surface membranes of the schistosomula of S. mansoni and found no evidence for internalization of these complexes.…”

“…Ligand-induced modulation of surface membrane determinants is a common event in many motile eucaryoticcell systems. A variety of mammalian cells (Nicholson 1974,1976, Schreiner & Unanue 1976, invertebrate blood phagocytes (Yoshino 1986, Dageforde, Schmucker & Renwrantz 1986, and parasitic protozoa (Speer et al 1985) undergo the sequential processes of 'patching' and 'capping' following binding of specific multivalent ligands to surface receptors. The fluidity of the lipid bilayer plasma membrane permits the aggregation of ligand-linked receptors into island 'patches' that coalesce, usually forming a single 'cap'.…”