A thorough study of parasitic helminth antigens is a pre-requisite for control programmes based on accurate immunochemical diagnosis, protection by vaccination and perhaps immune modulation to diminish pathological sequelae. Studies should be directed at the identification of those stage- or age-specific surface, secreted and somatic antigens which are involved in the host-parasite interactions responsible for immunity and/or pathology. Current methods of diagnosis of parasitic infections often fail to detect low-level patent infections, which incurs the risk of having a reservoir capable of perpetuating infections. There is, then, an urgent requirement for accurate immunochemical diagnosis, to be used in association with, and for the evaluation of, drug treatment and vector elimination, in parasite control programmes. Given the high sensitivity of current immunoassay technology, the only bar to establishing the necessary immunological tests is the choice of suitably specific antigen/antibody systems. Assays designed to detect parasite products or antigens are a major priority, as they indicate current infection, whereas those which detect antibody only indicate exposure to infection, which may or may not be current. Surface and secreted antigens are the most likely targets for protective immune responses and thus form a logical focus for vaccine design. The cestodes, which present such strong evidence for immunity following natural infection, are likely to yield effective vaccines by modern procedures. Certain antigens must, however, stimulate the humoral and/or cellular responses which are responsible for the undesirable immunopathological consequences of many helminthic diseases. The nematodes and trematodes furnish some extreme examples of such pathology. The ultimate objective in identifying these particular antigens is to utilize them in the appropriate down-regulation of the immune response responsible for such pathology. As an illustration, we have presented an interesting correlation between one particular clinical condition of onchocerciasis (Sowda) and the serological response, defined both in terms of the parasite antigens and an immunoglobulin class-restricted antibody response. Finally, the complexity of these parasite systems and the host response to the parasite should not be underestimated. Modern analytical techniques allow their detailed analysis in terms of the humoral antibody responses and afford the possibility of the future development of control and disease management procedures tailored to each individual host-parasite system. However, novel systems are required to complete the analysis of the cellular components of the immune response to parasite antigens, and functional studies are needed to determine the role that these parasite antigens play in the complex interaction between parasite and host.

The paper describes the development and analysis of a mathematical framework for the study of the within-host population dynamics of the interaction between macroparasites and the human immune system. Simple models of this interaction based on the proliferation of T cell clones specific to parasite antigen, and the impact of clonal expansion on parasite survival, capture the basic features of age-related changes in worm loads within human communities. The model is generalized to multiple epitopes on a single antigen, and reveals competitive exclusion amongst T cells, with a single clone becoming immunodominant in the absence of cross-reactive responses and genetic variation. The introduction of genetic heterogeneity and concomitant variability in the immunogenicity of specific epitopes induces additional complexity into the dynamical interaction. Most importantly, multiple epitope models with antigenic variation suggest that the immunodominant response may not necessarily be targeted at the epitope at which some strains show the greatest immunogenicity. High immunogenicity at a particular epitope can be masked by genetic variability even though many of the variants are more immunogenic at this epitope by comparison with the epitope to which the immunodominant immunological response is directed.