drosomycin [12] and metchnikowin [13]. Furthermore, the Drosophila
immune system seems to be capable of recognizing elements of
fungal virulence and triggering the Toll pathway via another protease,
called Persephone, independent of the GNBP-3 mechanism [14]. This
microbial-specific response seems to apply to systemic infections, while
in epithelial infections the Imd pathway seems to coordinate Drosophila
defense [15–17]. Newer studies have also shown the importance of pathways
not related to either Toll or Imd in the immune response of the fruit
fly, like the JNK and the JAK/STAT pathways [18]. Further, Chen et al.
showed that the p38 pathway that is part of the Toll cascade inmammals
participates in the immune response of Drosophila independent of the
Toll pathway, by up-regulating the expression of heat-shock proteins
and suppressing JNK activity [19]. It is important to note, however, that
despite similarities in the innate immune response between the fruit
fly and humans, there are many differences that pose serious limitations
to themodel. First, Drosophila does not have an adaptive immune system
and lacks antibodies. Additionally, its innate immune system lacks natural
killer cells, dendritic cells and cytokines that play a crucial role in the
human immune response. Finally, the fruit fly cannot be easily used as a
model system for tissue-specific infections in humans.