MECHANISMS OF EVASION OF SCHISTOSOMA MANSONI-SCHISTOSOMULA TO THE LETHAL ACTIVITY OF COMPLEMENT

Schistosomula of Schistosoma mansoni became resistant to antibody-depe ndent complement damage in vitro after pre-incubation with normal huma n erythrocytes (NHuE) whatever the ABO or Rh blood group. Resistant pa rasites were shown to acquire host decay accelerating factor (DAF), a 70 kDa glycoprotein attached to the membrane of NHuE by a GPI anchor. IgG2a mAb anti-human DAF (IA10) immunoprecipitated a 70 kDa molecule f rom I-125-labeled shistosomula pre-incubated with NHuE and inhibited t heir resistance to complement-dependent killing in vitro. Incubation o f schistosomula with erythrocytes from patients with paroxismal noctur nal hemoglobinuria (PNHE) or SRBC, which are DAF-deficient, did not pr otect the parasites from complement lesion. Supernatant of 100,000 x g collected from NHuE incubated for 24 h in defined medium was shown to contain a soluble form of DAF and to protect schistosomula from compl ement killing. Schistosomula treated with trypsin before incubation wi th NHuE ghosts did not become resistant to complement damage. On the o ther hand, pre-treatment with chymotrypsin did not interfere with the acquisition of resistance by the schistosomula. These results indicate that, in vitro, NHuE DAF can be transferred to schistosomula in a sol uble form and that the binding of this molecule to the parasite surfac e is dependent upon trypsin-sensitive chymotrypsin-insensitive polypep tide(s) present on the surface of the worm.