Overview of the Drosophila Immune Response

Drosophila has a multi-layered system for host defense. The chitin-based exoskel-eton and chitinous internal structures form a physical barrier. If a pathogen breaches these barriers, several immune effector mechanism respond, including cellular responses (i.e. phagocytosis, encapsulation, melanization) and humoral responses (i.e. antimicrobial peptides). Antimicrobial peptides are found both locally, at the site of infections, and systemically in the insect sera, or hemolymph. In terms of the systemic humoral response, the fat body is the major site of antimicrobial peptide production, although other tissues also contribute, including the malphigian tubules and circulating blood cells, known as hemocytes. The local response induces antimicrobial peptide gene expression in epithelial tissues, like the trachea and the gut (Ferrandon et al. 1998; Liehl et al. 2006; Tzou et al. 2000). Recognition is the first step in a cascade of events that leads to these immune responses. Microbial products, often cell wall components, are detected by recognition receptors, which in turn stimulate signaling pathways that culminate in the induction of antimicrobial peptide gene expression.

At least two different pathways regulate the expression of antimicrobial peptide genes in Drosophila. The Toll pathway is stimulated by fungal and many Grampositive bacterial pathogens. In contrast, the immune deficiency (IMD) pathway is triggered by Gram-negative bacteria. These two pathways are the focus of this chapter. In addition, we also discuss the Drosophila Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, which is implicated in immunity, although its role is less clear.

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