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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
2005-4-21
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pubmed:abstractText |
IL-18 is an essential cytokine for both innate and adaptive immunity. Signaling by IL-18 requires IL-18Ralpha, which binds specifically to the ligand and contains sequence homology to IL-1R and TLRs. It is well established that IL-1R signaling requires an accessory cell surface protein, AcP. Other accessory proteins also exist with roles in regulating TLR signaling, but some have inhibitory functions. An AcP-like molecule (AcPL) has been identified with the ability to cooperate with IL-18Ralpha in vitro; however, the physiological function of AcPL remains unknown. In this study, we demonstrate that IL-18 signals are abolished in AcPL-deficient mice and cells. Splenocytes from mutant mice fail to respond to IL-18-induced proliferation and IFN-gamma production. In particular, Th1 cells lacking AcPL fail to produce IFN-gamma in response to IL-18. AcPL-deficient neutrophils also fail to respond to IL-18-induced activation and cytokine production. Furthermore, AcPL is required for NK-mediated cytotoxicity induced by in vivo IL-18 stimulation. However, AcPL is dispensable for the activation or inhibition of IL-1R and the various TLR signals that we have examined. These results suggest that AcPL is a critical and specific cell surface receptor that is required for IL-18 signaling.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18 Receptor beta Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5351-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15843532-Animals,
pubmed-meshheading:15843532-Breeding,
pubmed-meshheading:15843532-Cell Differentiation,
pubmed-meshheading:15843532-Cytokines,
pubmed-meshheading:15843532-Cytotoxicity, Immunologic,
pubmed-meshheading:15843532-Gene Targeting,
pubmed-meshheading:15843532-Injections, Intraperitoneal,
pubmed-meshheading:15843532-Interferon-gamma,
pubmed-meshheading:15843532-Interleukin-18,
pubmed-meshheading:15843532-Interleukin-18 Receptor beta Subunit,
pubmed-meshheading:15843532-Killer Cells, Natural,
pubmed-meshheading:15843532-Membrane Glycoproteins,
pubmed-meshheading:15843532-Mice,
pubmed-meshheading:15843532-Mice, Knockout,
pubmed-meshheading:15843532-Neutrophil Activation,
pubmed-meshheading:15843532-Receptors, Cell Surface,
pubmed-meshheading:15843532-Receptors, Interleukin,
pubmed-meshheading:15843532-Receptors, Interleukin-1,
pubmed-meshheading:15843532-Recombination, Genetic,
pubmed-meshheading:15843532-Signal Transduction,
pubmed-meshheading:15843532-Spleen,
pubmed-meshheading:15843532-Th1 Cells,
pubmed-meshheading:15843532-Toll-Like Receptors
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pubmed:year |
2005
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pubmed:articleTitle |
Accessory protein-like is essential for IL-18-mediated signaling.
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pubmed:affiliation |
Advanced Medical Discovery Institute/Campbell Family Institute for Breast Cancer Research, University Health Network and Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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