Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-6-20
pubmed:abstractText
NK T (NKT) cells are an important component of the innate immune system and recognize the MHC class I-like CD1d molecule. NKT cells possess significant immunoregulatory activity due to their rapid secretion of large quantities of pro- and anti-inflammatory cytokines following CD1d-dependent stimulation. Because the innate immune system is programmed to respond to a multitude of diverse stimuli and must be able to quickly differentiate between pathogenic and endogenous signals, we hypothesized that, apart from stimulation via the TCR (e.g., CD1d-dependent activation), there must be multiple activation pathways that can be triggered through other cell surface receptors on NKT cells. Therefore, we analyzed the ability of CD44, a structurally diverse cell surface receptor expressed on most cells, to stimulate murine NKT cells, compared with conventional T cells. Stimulation of CD44 through Ab cross-linking or binding to its natural ligands hyaluronan and osteopontin induced NKT cells to secrete cytokines, up-regulate activation markers, undergo morphological changes, and resist activation-induced cell death, whereas conventional T cells only exhibited changes in morphology and protection from activation-induced cell death. This CD44-specific stimulation of NKT cells correlated with their ability to bind hyaluronan. Thus, fundamental differences in CD44 function between these lymphocyte subsets suggest an important biological role for CD44 in the innate immune response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
268-79
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16785522-Animals, pubmed-meshheading:16785522-Antibody Specificity, pubmed-meshheading:16785522-Antigens, CD44, pubmed-meshheading:16785522-Binding Sites, pubmed-meshheading:16785522-CD4-Positive T-Lymphocytes, pubmed-meshheading:16785522-Cell Death, pubmed-meshheading:16785522-Cross-Linking Reagents, pubmed-meshheading:16785522-Female, pubmed-meshheading:16785522-Hyaluronic Acid, pubmed-meshheading:16785522-Hybridomas, pubmed-meshheading:16785522-Isoantibodies, pubmed-meshheading:16785522-Killer Cells, Natural, pubmed-meshheading:16785522-Ligands, pubmed-meshheading:16785522-Lymphocyte Activation, pubmed-meshheading:16785522-Mice, pubmed-meshheading:16785522-Mice, Inbred C57BL, pubmed-meshheading:16785522-Mice, Knockout, pubmed-meshheading:16785522-T-Lymphocyte Subsets
pubmed:year
2006
pubmed:articleTitle
CD44 differentially activates mouse NK T cells and conventional T cells.
pubmed:affiliation
Department of Microbiology and Immunology, Indiana University School of Medicine, and Walther Oncology Center, Walther Cancer Institute, Indianapolis, IN 46208, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural