Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-5-2
pubmed:abstractText
The immune system in early life is regarded as immature. However, the IL-12 family member IL-23 is highly produced upon TLR stimulation by neonatal DCs. Human adult V?9V?2 T cells can be stimulated specifically via their TCR by phosphoantigens (as the pathogen-derived HMB-PP) or agents and infections that lead to their endogenous accumulation (as the aminobisphosphonate zoledronate). As increasing evidence indicates that ?? T cells are especially important in early life, we investigated the effect of IL-23 on neonatal V?9V?2 T cells stimulated via their TCR. Zoledronate induced clear proliferation and IFN-? production in neonatal V?9V?2 T cells. In contrast, HMB-PP did not elicit a distinct response unless at high concentrations. Addition of IL-23 to zoledronate enhanced the expression of IFN-? and generated a distinct, IFN-?-negative, neonatal V?9V?2 T cell population producing IL-17. Furthermore, IL-23 significantly enhanced the expression of a range of cytotoxic mediators (perforin, granzymes, granulysin). Although the costimulatory effect of IL-23 on IFN-? and cytotoxic mediators was also observed within adult V?9V?2 T cells, the induction of an IL-17+IFN-?- subset was unique to neonatal V?9V?2 T cells. In conclusion, neonatal DC-derived IL-23 combined with specific TCR signaling drives the generation of neonatal V?9V?2 T cells equipped with a range of cytotoxic mediators and distinct subpopulations producing IFN-? and IL-17.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation..., http://linkedlifedata.com/resource/pubmed/chemical/Diphosphonates, http://linkedlifedata.com/resource/pubmed/chemical/GNLY protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Granzymes, http://linkedlifedata.com/resource/pubmed/chemical/IL23R protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17, http://linkedlifedata.com/resource/pubmed/chemical/Perforin, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell..., http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin, http://linkedlifedata.com/resource/pubmed/chemical/T-cell receptor Vdelta2, human, http://linkedlifedata.com/resource/pubmed/chemical/T-cell receptor Vgamma9, human, http://linkedlifedata.com/resource/pubmed/chemical/zoledronic acid
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1938-3673
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
743-52
pubmed:meshHeading
pubmed-meshheading:21330350-Adult, pubmed-meshheading:21330350-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:21330350-Cell Proliferation, pubmed-meshheading:21330350-Cells, Cultured, pubmed-meshheading:21330350-Dendritic Cells, pubmed-meshheading:21330350-Diphosphonates, pubmed-meshheading:21330350-Flow Cytometry, pubmed-meshheading:21330350-Genes, T-Cell Receptor, pubmed-meshheading:21330350-Granzymes, pubmed-meshheading:21330350-Humans, pubmed-meshheading:21330350-Imidazoles, pubmed-meshheading:21330350-Infant, Newborn, pubmed-meshheading:21330350-Interferon-gamma, pubmed-meshheading:21330350-Interleukin-17, pubmed-meshheading:21330350-Perforin, pubmed-meshheading:21330350-Receptors, Antigen, T-Cell, gamma-delta, pubmed-meshheading:21330350-Receptors, Interleukin, pubmed-meshheading:21330350-Signal Transduction, pubmed-meshheading:21330350-T-Lymphocyte Subsets
pubmed:year
2011
pubmed:articleTitle
IL-23R and TCR signaling drives the generation of neonatal Vgamma9Vdelta2 T cells expressing high levels of cytotoxic mediators and producing IFN-gamma and IL-17.
pubmed:affiliation
Institute for Medical Immunology, Université Libre de Bruxelles, Gosselies, Belgium.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't