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pubmed-article:21330350pubmed:dateCreated2011-5-2lld:pubmed
pubmed-article:21330350pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:21330350pubmed:authorpubmed-author:GoldmanMichel...lld:pubmed
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pubmed-article:21330350pubmed:articleTitleIL-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.lld:pubmed
pubmed-article:21330350pubmed:affiliationInstitute for Medical Immunology, Université Libre de Bruxelles, Gosselies, Belgium.lld:pubmed
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pubmed-article:21330350pubmed:publicationTypeComparative Studylld:pubmed
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