Parasite immune evasion and exploitation: reflections and projections.
Recent developments in parasite immune evasion and exploitation are reviewed with special reference to the papers presented in this volume. Parasites, broadly defined, of animals with good immune responses have evolved many strategies that adapt them to survive and reproduce. These strategies may be passive, or may involve active intervention with host immune regulation, and can be categorized as immune evasion, immune exploitation and molecular piracy. The concept of immune evasion began with Paul Ehrlich's demonstration of antigenic variation in African trypanosomes and was reinforced by later ideas on molecular mimicry. Molecular mimicry is updated in the light of recent discoveries about degeneracy and plasticity of TCR/MHC-peptide recognition. Possible connections between two of its postulated consequences, evasion and autoimmunity, are discussed. Another putative consequence of molecular mimicry, host antigenic polymorphism, is also updated. The concept of exploitation of host immune responses by parasites has been reinforced by new data on its first known examples, especially the immune dependence of schistosome egg excretion. Newer examples include use of host cytokines as parasite growth factors, virokines, viroreceptors and helminth pseudocytokines. Finally, questions of host gene capture by viruses and possible horizontal gene transfer between host and parasite mediated by retroviruses are examined. The latter is compared with molecular conservation as a source of molecular mimicry and other aspects of host--parasite coevolution.
Damian
R T
RT
Department of Cellular Biology, University of Georgia, Athens 30602, USA.
D000818:Animals; D015551:Autoimmunity; D005075:Biological Evolution; D006790:Host-Parasite Interactions; D006801:Humans; D018716:Molecular Mimicry; D010271:Parasites / Q000235:genetics / Q000276:immunology* / Q000502:physiology; D010272:Parasitic Diseases / Q000276:immunology* / Q000469:parasitology