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Excretory–secretory products of helminth parasites: effects on host immune responses

Published online by Cambridge University Press:  23 August 2011

M. W. Lightowlers
Affiliation:
University of Melbourne, Veterinary Clinical Centre, Princes Highway, Werribee, Victoria, Australia 3030
M. D. Rickard
Affiliation:
University of Melbourne, Veterinary Clinical Centre, Princes Highway, Werribee, Victoria, Australia 3030

Summary

Parasitic helminths excrete or secrete (ES) a variety of molecules into their mammalian hosts. The effects of these ES products on the host's immune responses are reviewed. Investigations into the source of antigenic or immunoregulatory ES products have identified the cuticular and tegumental surfaces of some nematodes and trematodes respectively as being important sources of ES products; other ES molecules are released through specialized excretory or secretory organs. It is proposed that the active shedding of surface antigens may serve as an important source of parasite antigens available to the immune system in a form in which they can be taken up and processed by antigen-presenting dendritic cells, macro-phages and certain B cells for presentation to T helper cells. The ES products of nematodes, trematodes and cestodes contribute to immune evasion strategies of the parasites through mechanisms including shedding of surface-bound ligands and cells, alteration of lymphocyte, macrophage and granulocyte functions and modulation of complement and other host inflammatory responses. Immunopathology may be induced by ES products as in the development of granulomas around entrapped schistosome eggs. In some host – parasite systems ES antigens may induce host-protective immune responses and this source of protective antigens has been utilized in the successful vaccination against helminth infections, particularly against infection with trichurid nematodes and the metacestode stage of cestode parasites. The use of ES antigens in immunodiagnosis of helminth infection is also briefly discussed.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1988

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References

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