Arabidopsis thaliana can reveal pathogenetic strategies of bacteria, Dictyostelium discoideum can serve as a surrogate macrophage, Caenorhabditis elegans and Droso-phila melanogaster are established models of innate immune function, and Danio rerio and Mus musculus are suited to the study of both innate and adaptive immunity (table 20.1). With the determination of the genomes of both pathogen and host, and an impressive toolbox including microarrays and proteomic analysis, it is envisaged that a comprehensive understanding of the respective interactions is at hand. A common reproach against these model systems is that they do not represent a real human infection. In the present review we set out to demonstrate that model systems can indeed sometimes better model selected aspects of bacteria-host interactions. A prerequisite for this, however, is that conclusions drawn from model organisms take into account that fact that certain properties are not represented in the model and some model properties cannot be found in the real system. In consequence, the selection of an appropriate model organism with an appropriate level of complexity appears to be essential to elaborate valid results. In the past a combination of different complementary model systems has proven helpful. The Toll proteins, for instance, were originally identified in Drosophila mutants. Further members of this protein family and important agonists have later been identified in mice. Meanwhile, related genes that recognize pathogen-associated molecular patterns have also been identified in humans. This demonstrates that rapid advances can be achieved by the translation of knowledge acquired through the study of model organisms.
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