MIicrobial pathogens can invade their hosts through a variety of routes, but one path is to sneak in through an open wound in the external body surface. To stave off these microbial invaders, hosts can sense a breach in the epidermal barrier and rapidly upregulate antimicrobial defenses1'2. The nematode Caenorhabditis elegans responds to both wounding and pathogen infection by rapidly inducing the expression of genes that encode antimicrobial molecules, but the ligands and receptors that trigger this induction have remained elusive. In this issue of Nature Immunology, Zugasti et al. show that C. elegans appears to sense both wounding and fungal infection with an epidermally expressed G protein-coupled receptor (GPCR) that is activated by an endogenous ligand to trigger innate immune responses.
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