[
Immunogenetics,
2000]
Toll receptor systems play an important role in our innate immune response to microbial infection (Rock et al. 1998). Studies of related pathways in arthropods (Hoffmann et all. 1999; Imler and Hofmann 2000) have led to key advances in our understanding of these processes. Until recently, however, the possibility that Toll signals may activate both immune and/or developmental pathways in Caenorhabditis elegans has been largely ignored. Early failures to identify Toll receptors or NFB-like transcription factors in the C. elegans genome (Ruvkun and Hobert 1998) let to the assumption that its Toll pathway was inoperable. Therefore, given the paucity of knowledge on innate immune responses for these animals, there was no impetus to develop C. elegans pathogenicity models. Recent database searches, however, have identified components of the elusive C. elegans Toll receptor pathway (Rich et al. 2000; Tan et al. 1999). The existence of a rudimentary immune response is further supported by evidence that antimicrobial peptides are encoded within the C. elegans genome (Tan and Ausubel 2000). In fact, C. elegans is susceptible to infection from several different pathogens, making this genetically tractable invertebrate an attractive model to study host-pathogen interactions. These developments are particularly important for the study of pathogens such as Pseudomonas aeruginosa whose natural hosts include humans. A suitable C. elegans model could, for example, provided a rapid system to screen candidate antibacterial drugs. Consequently, it has now become important to identify and isolate cDNAs for each component of the C. elegans Toll pathway.