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- Daniela Wesch
- Institute of Immunology, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany
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- Susann Beetz
- Institute of Immunology, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany
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- Hans-Heinrich Oberg
- Institute of Immunology, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany
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- Matthias Marget
- Institute of Immunology, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany
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- Kirsten Krengel
- Institute of Immunology, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany
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- Dieter Kabelitz
- Institute of Immunology, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany
説明
<jats:title>Abstract</jats:title><jats:p>TLR3 recognizes viral dsRNA and its synthetic mimetic polyinosinic-polycytidylic acid (poly(I:C)). TLR3 expression is commonly considered to be restricted to dendritic cells, NK cells, and fibroblasts. In this study we report that human γδ and αβ T lymphocytes also express TLR3, as shown by quantitative real-time PCR, flow cytometry, and confocal microscopy. Although T cells did not respond directly to poly(I:C), we observed a dramatic increase in IFN-γ secretion and an up-regulation of CD69 when freshly isolated γδ T cells were stimulated via TCR in the presence of poly(I:C) without APC. IFN-γ secretion was partially inhibited by anti-TLR3 Abs. In contrast, poly(I:C) did not costimulate IFN-γ secretion by αβ T cells. These results indicate that TLR3 signaling is differentially regulated in TCR-stimulated γδ and αβ T cells, suggesting an early activation of γδ T cells in antiviral immunity.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 176 (3), 1348-1354, 2006-02-01
Oxford University Press (OUP)