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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Tenor, JL; Aballay, A

Published Date

  • January 2008

Published In

Volume / Issue

  • 9 / 1

Start / End Page

  • 103 - 109

PubMed ID

  • 17975555

Pubmed Central ID

  • 17975555

Electronic International Standard Serial Number (EISSN)

  • 1469-3178

International Standard Serial Number (ISSN)

  • 1469-221X

Digital Object Identifier (DOI)

  • 10.1038/sj.embor.7401104

Language

  • eng