A conserved Toll-like receptor is required for Caenorhabditis elegans innate immunity

Pathogen recognition through Toll‐like receptors (TLRs) is crucial in order to mount an appropriate immune response against microorganisms. On the basis of a lack of evidence indicating that Caenorhabditis elegans uses TLRs to elicit an immune response and on the absence of genes encoding Rel‐like transcription factors in its genome, it is believed that TLR‐mediated immunity arose after coelomates split from pseudocoelomates and acoelomates. Here, we show that C. elegans tol‐1 ( nr2033 ) mutants are killed by the human pathogen Salmonella enterica , which causes a significant pharyngeal invasion in the absence of TOL‐1‐mediated immunity. We also show that TOL‐1 is required for the correct expression of ABF‐2, which is a defensin‐like molecule expressed in the pharynx, and heat‐shock protein 16.41, which is also expressed in the pharynx and is part of a HSP family of proteins required for C. elegans immunity. The results indicate that TOL‐1 has a direct role in defence response to certain Gram‐negative bacteria and indicate that part of the TLR‐mediated immunity might be evolutionarily conserved.