Editors' ChoiceInnate Immunity

No Toll for Worm Immunity

Science's STKE  21 Jan 2003:
Vol. 2003, Issue 166, pp. tw30-TW30
DOI: 10.1126/stke.2003.166.tw30

The toll-like receptors (TLRs) function in innate immunity in mammals and flies, but how about in worms? Aballay et al. studied the innate immune response of Caenorhabditis elegans to infection with Salmonella, which causes programmed cell death of gonadal cells. Although worms have a Toll-like receptor, mutants lacking that receptor or lacking the worm homologs of TRAF1 (tumor necrosis factor receptor-associated protein 1) or IRAK (interleukin-1 receptor-associated kinase) (both signaling proteins activated in response to TLRs in mammals), the gonadal cells still underwent programmed cell death normally in infected animals. One signaling component that was conserved in the worm immune response was PMK-1, the homolog of p38 mitogen-activated protein kinase (MAPK). Because signals upstream and downstream of p38 MAPK differ from those in mammals, the authors propose that p38 MAPK cascade may be the oldest conserved part of the innate immune response to Gram-negative bacteria.

A. Aballay, E. Drenkard, L. R. Hilbun, F. M. Ausubel, Caenorhabditis elegans innate immune response triggered by Salmonella enterica requires intact LPS and is mediated by a MAPK signaling pathway. Curr. Biol. 13, 47-52 (2003) [Online Journal]