Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-1-6
pubmed:abstractText
NKT cells recognize lipid Ags presented by CD1d molecules and play an important role in the regulation of innate and adaptive immune responses. In this study, we report the identification of a membrane-associated protein, Ig-like transcript 4 (ILT4), as a novel human CD1d receptor that inhibits CD1d-mediated immune responses. We found that native CD1d tetramer generated by mammalian cells was able to specifically bind human monocytes in the peripheral blood, and this binding was at least partly mediated by monocyte-expressed ILT4. The interaction between ILT4 and CD1d involves the two N-terminal domains of ILT4 and the Ag-binding groove of CD1d (alpha1/alpha2 domain). This interaction has been identified on the cell surface as well as in the endosomal and lysosomal compartments. Functional analysis showed that ILT4 could block the loading of lipid Ags such as alpha-GalCer, and consequently inhibited NKT recognition. The interaction between ILT4 and CD1d may provide new insights into the regulation of NKT-mediated immunity.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-10050671, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-10190906, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-10764620, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-11114384, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-11169396, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-11698424, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-12390682, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-12853576, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-12897781, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-14684827, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-14716312, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-14722359, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-15032598, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-15771592, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-15928680, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-16007090, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-16087713, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-16311334, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-17056715, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-17150027, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-17403933, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-17428648, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-17581592, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-18037897, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-18068183, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-18645582, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-8810254, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-9285411, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-9382880, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-9488653, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-9531263, http://linkedlifedata.com/resource/pubmed/commentcorrection/19124746-9933109
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
182
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1033-40
pubmed:dateRevised
2010-9-23
pubmed:meshHeading
pubmed-meshheading:19124746-Animals, pubmed-meshheading:19124746-Antigen Presentation, pubmed-meshheading:19124746-Antigen-Presenting Cells, pubmed-meshheading:19124746-Antigens, CD1d, pubmed-meshheading:19124746-Cell Line, pubmed-meshheading:19124746-Cell Membrane, pubmed-meshheading:19124746-Cells, Cultured, pubmed-meshheading:19124746-Cytoplasm, pubmed-meshheading:19124746-Galactosylceramides, pubmed-meshheading:19124746-Humans, pubmed-meshheading:19124746-Immune Tolerance, pubmed-meshheading:19124746-Immunity, Cellular, pubmed-meshheading:19124746-Lymphocyte Activation, pubmed-meshheading:19124746-Membrane Glycoproteins, pubmed-meshheading:19124746-Monocytes, pubmed-meshheading:19124746-Protein Binding, pubmed-meshheading:19124746-Rats, pubmed-meshheading:19124746-Receptors, Immunologic
pubmed:year
2009
pubmed:articleTitle
Ig-like transcript 4 inhibits lipid antigen presentation through direct CD1d interaction.
pubmed:affiliation
Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Headington, Oxford, UK. demin.li@imm.ox.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't