Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-11-5
pubmed:abstractText
CD8(+) natural killer T (NKT) cells from EBV-associated tumour patients are quantitatively and functionally impaired. EBV-induced CD8(+) NKT cells drive syngeneic T cells into a Th1-bias response to suppress EBV-associated malignancies. IL-4-biased CD4(+) NKT cells do not affect either syngeneic T cell cytotoxicity or Th cytokine secretion. Circulating mDC1 cells from patients with EBV-associated malignancies impair the production of IFN-gamma by CD8(+) NKT cells. In this study, we have established a human-thymus-SCID chimaera model to further investigate the underlying mechanism of EBV-induced CD8(+) NKT cells in suppressing EBV-associated malignancies. In the human-thymus-SCID chimera, EBV-induced CD8(+) NKT cells suppress EBV-associated malignancies in a manner dependent on the Th1-bias response and syngeneic CD3(+) T cells. However, adoptive transfer with CD4(+) NKT cells alone inhibits T cell immunity. Interestingly, CD4(+) NKT cells themselves secrete high levels of IL-2, enhancing the persistence of adoptively transferred CD8(+) NKT cells and T cells, thereby leading to a more pronounced T cell anti-tumour response in chimaeras co-transferred with CD4(+) and CD8(+) NKT cells. Thus, immune reconstitution with EBV-induced CD4(+) and CD8(+) NKT cells synergistically enhances T cell tumour immunity, providing a potential prophylactic and therapeutic treatment for EBV-associated malignancies.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
2042-0226
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
367-79
pubmed:dateRevised
2011-8-19
pubmed:meshHeading
pubmed-meshheading:19887050-Adoptive Transfer, pubmed-meshheading:19887050-Animals, pubmed-meshheading:19887050-Antigens, CD4, pubmed-meshheading:19887050-Antigens, CD8, pubmed-meshheading:19887050-Cell Line, Tumor, pubmed-meshheading:19887050-Chimera, pubmed-meshheading:19887050-Cytotoxicity, Immunologic, pubmed-meshheading:19887050-Epstein-Barr Virus Infections, pubmed-meshheading:19887050-Herpesvirus 4, Human, pubmed-meshheading:19887050-Hodgkin Disease, pubmed-meshheading:19887050-Humans, pubmed-meshheading:19887050-Interferon-gamma, pubmed-meshheading:19887050-Interleukin-2, pubmed-meshheading:19887050-Interleukin-4, pubmed-meshheading:19887050-Lymphocyte Activation, pubmed-meshheading:19887050-Lymphoma, B-Cell, pubmed-meshheading:19887050-Mice, pubmed-meshheading:19887050-Mice, SCID, pubmed-meshheading:19887050-Nasopharyngeal Neoplasms, pubmed-meshheading:19887050-Natural Killer T-Cells, pubmed-meshheading:19887050-T-Lymphocyte Subsets, pubmed-meshheading:19887050-Th1 Cells
pubmed:year
2009
pubmed:articleTitle
EBV-induced human CD8(+) NKT cells synergise CD4(+) NKT cells suppressing EBV-associated tumours upon induction of Th1-bias.
pubmed:affiliation
Laboratory of Allergy and Clinical Immunology, Institute of Allergy and Immune-related Diseases, Center for Medical Research, and Department of Immunology, Wuhan University School of Medicine, Wuhan, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't