How Schistosoma mansoni evades complement-mediated immune attack

Schistosoma mansoni is a trematode that parasitizes man and other mammals, surviving in the vertebrate host for decades, despite eliciting a strong cellular and humoral immune response. The mechanism by which S. mansoni evades immune attack, even in the presence of specific antischistosome antibodies and complement has been the object of perplexity. It was originally proposed that schistosomes avoid antibody recognition by masking themselves with host antigens, and erythrocyte-derived molecules have been appointed as playing this role. We have discovered that schistosomula become complement-resistant by incorporating into their surface a complement inhibitory molecule released from human erythrocytes (HuE). This molecule was shown to be the decay-accelerating factor (DAF), a 70 kDa protein tethered to the surface of HuE by a glycosylphosphatidylinositol (GPI) anchor. The mechanism by which schistosomula acquire DAF from the surface of HuE and its importance to the survival of S.mansoni in the host are discussed.

Decay accelerating factor (DAF) as the host antigen with protective activity to complement killing of schistosomula

The acquisition of host antigens by Schistosoma mansoni was studied by evaluating the resistance of schistosomula to the complement attack mediated by lethal antibody. Schistosomula cultured for 24 hours with intact human erythrocytes (N-HuE) or ghosts of any type of ABO or Rh blood group, showed a marked resistance to complement damage. Sheep red blood cells, pronase-treated N-HuE or erythrocytes from patients with paroxysmal nocturnal hemoglobinuria, which are complement-sensitive cells, were unable to protect schistosomula. Schistosomula protected by N-HuE became again susceptible to complement killing after incubation with a monoclonal antibody anti-DAF. These results indicate that, in vitro, host DAF from N-HuE can be acquired by schistosomula surface in a biological active form that protects the parasite from the complement lesion.