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

@article{citeulike:3335932, abstract = {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.}, author = {Tenor, J. L. and Aballay, A.}, citeulike-article-id = {3335932}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/17975555}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=17975555}, citeulike-linkout-2 = {http://www.wormbase.org/db/misc/paper?name=WBPaper00031161}, journal = {EMBO Rep}, keywords = {abf-2, b02183, c04f123, c07f111, c50f210, c\_elegans, caenorhabditis\_elegans, celegans, dbl-1, elegans, f45g26, hsp-1641, ikb-1, nematode, other, pmk-1, t25f102, tol-1, trf-1, wormbase, y46h3a2}, posted-at = {2008-09-25 14:41:35}, priority = {3}, title = {A conserved Toll-like receptor is required for Caenorhabditis elegans innate immunity.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/17975555}, year = {2007} }

TY - JOUR ID - citeulike:3335932 L3 - citeulike-article-id:3335932 N2 - 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. JF - EMBO Rep TI - A conserved Toll-like receptor is required for Caenorhabditis elegans innate immunity. KW - abf-2 KW - b02183 KW - c04f123 KW - c07f111 KW - c50f210 KW - c_elegans KW - caenorhabditis_elegans KW - celegans KW - dbl-1 KW - elegans KW - f45g26 KW - hsp-1641 KW - ikb-1 KW - nematode KW - other KW - pmk-1 KW - t25f102 KW - tol-1 KW - trf-1 KW - wormbase KW - y46h3a2 AU - Tenor, JL AU - Aballay, A PY - 2007/// UR - http://view.ncbi.nlm.nih.gov/pubmed/17975555 ER -