Paired C-type lectin receptors mediate specific recognition of divergent oomycete pathogens inC. elegans

Abstract

SummaryInnate immune responses can be initiated through the detection of pathogen or damage-associated molecular patterns by host receptors that are often present on the surface of immune cells. While certain invertebrates likeCaenorhabditis eleganslack professional immune cells, they still respond to infection in a pathogen-specific manner. It has been debated for years whether homologues of the canonical pathogen recognition receptors are also functioning in the nematode. Here we show that C-type lectin receptors mediate species-specific recognition of divergent oomycetes inC. elegans.A CLEC-27/CLEC-35 pair is essential for recognition of the oomyceteMyzocytiopsis humicola, while a CLEC-26/CLEC-36 pair is required for detection ofHaptoglossa zoospora.Bothclecpairs are transcriptionally regulated through a shared promoter by the conserved PRD-like homeodomain transcription factor CEH-37/OTX2 and act in sensory neurons and the anterior intestine to trigger a protective immune response in the epidermis. This system enables redundant tissue sensing of oomycete threats through canonical CLEC receptors and host defense via cross-tissue communication.HighlightsA CLEC-27/CLEC-35 pair is required for recognition of the oomyceteMyzocytiopsis humicolaA CLEC-26/CLEC-36 pair is required for recognition of the oomyceteHaptoglossa zoosporaBoth CLEC pairs are co-regulated by the homeodomain transcription factor CEH-37/OTX2Both CLEC pairs function redundantly in sensory neurons and the intestine for host defense