Host antigens in schistosomiasis

Abstract

It has previously been shown that adult schistosomes excite an immune response in the rhesus monkey but do not themselves succumb to this response. Furthermore, schistosomes are known to persist in the blood of man and experimental animals for long periods. These findings point to the evolution of a special mechanism for circumventing the immune defences of the host. The present paper sets out evidence which suggests that this mechanism involves the incorporation of host antigens at the surface of the adult worm. When adult worms, which had been grown in mice (‘mouse worms’), were transferred into the hepatic portal systems of normal monkeys, a large proportion (84 %) were recovered alive 1 to 6 weeks later. Worms recovered after 1 week were pale and shrunken and the females had ceased egg production; worms recovered after 6 weeks were normal and egg production had been resumed. Evidently, the transferred worms find difficulty at first in adapting to their new host species, but in time they are able to adapt fully. In contrast, when mouse worms were transferred to monkeys previously immunized against normal mouse tissues (anti-mouse monkeys), very few of these worms survived. Indeed, when the monkeys were immunized against mouse spleen and liver cells or erythrocytes, combined with Freund’s complete adjuvant, the transferred mouse worms were completely destroyed. This result indicates that the worms grown in mice had mouse antigens closely associated with them, and that on transfer to anti-mouse monkeys, the worms were destroyed by the ensuing immunological reaction. This immunity was passively transferred to normal monkeys by means of serum; thus the immunity is largely antibody-mediated. Most of the mouse worms died between 7 and 25 h after transfer. The immune reaction was directed mainly against the tegument of the worm, causing breaks in the plasma mem­brane and vacuolation and subsequent degeneration of the underlying syncytium. The mixed agglutination reaction and the use of a ferritin-labelled antiserum combined with electron microscopy confirmed that host antigens were located at the surface of the worm. The antigens appear to be host species-specific; worms which were grown in monkeys or libyan jirds survived normally when transferred to anti-mouse monkeys. There is evidence that the antigens may readily be exchanged between host and parasites. Mouse worms which were transferred to a normal monkey and then transferred after 7 days to an anti-mouse monkey survived as well as monkey worms. Evidently the mouse worms had lost their mouse antigens during this period, perhaps exchanging them for monkey antigens. Three days in a normal monkey was not sufficient, however, for all of the mouse worms to lose their mouse antigens. It is suggested that these host antigens are synthesized by the host, but that they become firmly bound to or incorporated in the tegument. It is conceivable that these antigens serve to disguise the worms as host tissue, thus preventing their rejection by the immune defences of the host. This hypothesis provides an explanation for the apparent anomalies, referred to earlier: the insusceptibility of adult worms to the immune response which they are known to provoke, and their long persistence in the blood, an immunologically hostile environment.

Molecular parasitism in the Escherichia coli-Bdellovibrio bacteriovorus system: translocation of the matrix protein from the host to the parasite outer membrane.

“…The ability of Bdellovibrio to disguise itself within a 'host-like phenotype' could represent a step towards the evolution of a mechanism to escape the host's defense mechanisms. In fact, the appropriation of host proteins by Bdellovibrio may provide a model, useful for the interpretation of the widespread sharing of antigens between hosts and parasites (Damian, 1964;De Vay and Adler, 1976), not only as a consequence of evolutionary convergence of proteins but also via direct uptake of host antigens, as described in Schistosoma (Smithers et al, 1969;Clegg et al, 1971;Sher et al, 1978;Bloom, 1979).…”

Cloning of a cDNA encoding a surface antigen of Schistosoma mansoni schistosomula recognized by sera of vaccinated mice.

“…Because the 18-, 94-, 100-, and >300-kDa polypeptides are all accessible to surface iodination and share an epitope(s), they may each contribute to the fluorescence observed. In the case of liver-stage and adult worms the epitopes recognized by anti-654 were not accessible at the surface and may be masked by host molecules (22). This correlates with the insusceptibility of schistosomula to immune-dependent elimination following migration from the lungs (23).…”

Egg excretion patterns as criterion for the determination of prevalence and intensity of infection in male and female individuals in different age groups in a schistosome endemic area in the Limpopo Province

“…7 Hierdie verskynsel is waarskynlik toe te skryf aan mindere kontak met skistosoombesmette water sowel as aan die moontlikheid van konkomitante immuniteit wat impliseer dat besmette mense immuniteit teen herinfeksies opbou en dat hierdie immuniteit met ouderdom toeneem. 16 Die feit dat daar betekenisvol meer individue in die 10-14 jaar ouderdomsgroep teenwoordig was wat matige en swaar infeksies getoon het, was ook te wagte gesien in die lig van die feit dat dit die ouderdomsgroep is wat vanweë hulle waterkontakpatrone die groep is wat die hoogste risiko inhou om besmet te raak.…”