The US National Science Foundation has funded a Research Coordination Network to bring methodological and conceptual unity to the field of ecoimmunology.
The causes and consequences of immune variation have larger implications for public health, conservation, wildlife management, and agriculture.
[8] Folstad and Karter proposed the immunocompetence handicap hypothesis, whereby testosterone acts as a mediator of immunosuppression and thus keeps sexually-selected traits honest.
[7] Although there is only moderate observational or experimental evidence supporting this claim up until now, the paper itself was one of the first links to be made suggesting a cost to immunity requiring trade-offs between it and other physiological processes.
More recently, ecoimmunology has been the theme of three special issues in peer-reviewed journals, in Philosophical Transactions of the Royal Society B, in Functional Ecology, and in Physiological and Biochemical Zoology (see External links).
[12] Among organisms, in developmental stages, the allocation of energy toward immune function may trade-off with physical growth, particularly in environments characterized by high-pathogen and low resources.
[16] Trade-offs occur between bodily maintenance (which includes immune function) and reproduction, as metabolic energy expenditure is increased during pregnancy and lactation.
[22] A study of wild red deer on the Isle of Rum, off the coast of Scotland, found that reproducing females had lower antibody levels and higher parasite counts.
[7][24] Energetically expensive secondary sexual characteristics, such as skeletal muscle mass, have been shown to predict a relationship between testosterone levels and reproductive effort.
[25] This model considers the variability we see as a plastic response to environmental stimuli and disease risk in different ecological environments, fundamental shifts between energetic allocations from reproductive to somatic efforts.
[40] Self-medication, a form of host resistance, is defined as an individual response to infection through the ingestion or harvesting of non-nutritive compounds or plant materials.
[46] An example of this, Apis mellifera incorporate plant resins in their nest building as this can reduce the chronic elevation of an immune response at the individual level.
In animal models, fruit flies that were selected for parasitoid resistance showed reduced larval competitiveness only when they were subject to food limitations.
[52] For instance, commensal microbes influence the host's ability to survive pathogenic exposures through several mechanisms including inter-microbial competition and interaction with the immune system.
[16] Temperature stress has been causally linked to declines in immune function in several species including C. elegans, Daphnia magna, and Drosophila melanogaster.
[54] Segments of Neanderthal ancestry genomes introgressed to modern humans are enriched for proteins that interact with viruses suggestive of viral selection pressure throughout evolution.
[6] Another source of criticism comes from the need for to develop assays that can be utilized across species and be accessible in multiple laboratories due to the fact that ecoimmunologists primarily study non-model organisms.
[58] Models of host-pathogen coevolution have shown that the nature of life-history trade-offs can greatly alter the evolution of pathogen virulence and its ability to harm infected hosts.
[61] A shift in focus to tolerance rather than eradication might provide fruitful avenues for treatments that reduce virulence rather than eliminating parasites.