The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Giorgio Napolitani - One of the best experts on this subject based on the ideXlab platform.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of Interleukin 17–producing human T helper cells
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)-producing CD4(+) helper T cells (T(H)-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of T(H)-17 cells requires transforming growth factor-beta and IL-6 and the transcription factor RORgammat. We report here that for human naive CD4(+) T cells, RORgammat expression and T(H)-17 polarization were induced by IL-1beta and enhanced by IL-6 but were suppressed by transforming growth factor-beta and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced T(H)-17 priming, and this function correlated with antigen-presenting cell production of IL-1beta and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human T(H)-17 cells and emphasize an important difference in the requirements for the differentiation of T(H)-17 cells in humans and mice.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)–producing CD4+ helper T cells (TH-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of TH-17 cells requires transforming growth factor-β and IL-6 and the transcription factor RORγt. We report here that for human naive CD4+ T cells, RORγt expression and TH-17 polarization were induced by IL-1β and enhanced by IL-6 but were suppressed by transforming growth factor-β and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1β and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Surface phenotype and antigenic specificity of human Interleukin 17–producing T helper memory cells
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) have been characterized in mice as a distinct subset of effector cells, but their identity and properties in humans remain elusive. We report here that expression of CCR6 and CCR4 together identified human memory CD4+ T cells selectively producing IL-17 and expressing mRNA encoding the human ortholog of mouse RORgammat, a transcription factor, whereas CCR6 and CXCR3 identified T(H)1 cells producing interferon-gamma and T helper cells producing both interferon-gamma and IL-17. Memory T cells specific for Candida albicans were present mainly in the CCR6+CCR4+ T(H)-17 subset, whereas memory T cells specific for Mycobacterium tuberculosis were present in CCR6+CXCR3+ T helper type 1 subset. The elicitation of IL-17 responses correlated with the capacity of C. albicans hyphae to stimulate antigen-presenting cells for the priming of T(H)-17 responses in vitro and for the production of IL-23 but not IL-12. Our results demonstrate that human T(H)-17 cells have distinct migratory capacity and antigenic specificities and establish a link between microbial products, T helper cell differentiation and homing in response to fungal antigens.
Federica Sallusto - One of the best experts on this subject based on the ideXlab platform.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of Interleukin 17–producing human T helper cells
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)-producing CD4(+) helper T cells (T(H)-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of T(H)-17 cells requires transforming growth factor-beta and IL-6 and the transcription factor RORgammat. We report here that for human naive CD4(+) T cells, RORgammat expression and T(H)-17 polarization were induced by IL-1beta and enhanced by IL-6 but were suppressed by transforming growth factor-beta and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced T(H)-17 priming, and this function correlated with antigen-presenting cell production of IL-1beta and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human T(H)-17 cells and emphasize an important difference in the requirements for the differentiation of T(H)-17 cells in humans and mice.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)–producing CD4+ helper T cells (TH-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of TH-17 cells requires transforming growth factor-β and IL-6 and the transcription factor RORγt. We report here that for human naive CD4+ T cells, RORγt expression and TH-17 polarization were induced by IL-1β and enhanced by IL-6 but were suppressed by transforming growth factor-β and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1β and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Surface phenotype and antigenic specificity of human Interleukin 17–producing T helper memory cells
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) have been characterized in mice as a distinct subset of effector cells, but their identity and properties in humans remain elusive. We report here that expression of CCR6 and CCR4 together identified human memory CD4+ T cells selectively producing IL-17 and expressing mRNA encoding the human ortholog of mouse RORgammat, a transcription factor, whereas CCR6 and CXCR3 identified T(H)1 cells producing interferon-gamma and T helper cells producing both interferon-gamma and IL-17. Memory T cells specific for Candida albicans were present mainly in the CCR6+CCR4+ T(H)-17 subset, whereas memory T cells specific for Mycobacterium tuberculosis were present in CCR6+CXCR3+ T helper type 1 subset. The elicitation of IL-17 responses correlated with the capacity of C. albicans hyphae to stimulate antigen-presenting cells for the priming of T(H)-17 responses in vitro and for the production of IL-23 but not IL-12. Our results demonstrate that human T(H)-17 cells have distinct migratory capacity and antigenic specificities and establish a link between microbial products, T helper cell differentiation and homing in response to fungal antigens.
Eva V Acostarodriguez - One of the best experts on this subject based on the ideXlab platform.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of Interleukin 17–producing human T helper cells
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)-producing CD4(+) helper T cells (T(H)-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of T(H)-17 cells requires transforming growth factor-beta and IL-6 and the transcription factor RORgammat. We report here that for human naive CD4(+) T cells, RORgammat expression and T(H)-17 polarization were induced by IL-1beta and enhanced by IL-6 but were suppressed by transforming growth factor-beta and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced T(H)-17 priming, and this function correlated with antigen-presenting cell production of IL-1beta and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human T(H)-17 cells and emphasize an important difference in the requirements for the differentiation of T(H)-17 cells in humans and mice.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)–producing CD4+ helper T cells (TH-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of TH-17 cells requires transforming growth factor-β and IL-6 and the transcription factor RORγt. We report here that for human naive CD4+ T cells, RORγt expression and TH-17 polarization were induced by IL-1β and enhanced by IL-6 but were suppressed by transforming growth factor-β and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1β and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Surface phenotype and antigenic specificity of human Interleukin 17–producing T helper memory cells
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) have been characterized in mice as a distinct subset of effector cells, but their identity and properties in humans remain elusive. We report here that expression of CCR6 and CCR4 together identified human memory CD4+ T cells selectively producing IL-17 and expressing mRNA encoding the human ortholog of mouse RORgammat, a transcription factor, whereas CCR6 and CXCR3 identified T(H)1 cells producing interferon-gamma and T helper cells producing both interferon-gamma and IL-17. Memory T cells specific for Candida albicans were present mainly in the CCR6+CCR4+ T(H)-17 subset, whereas memory T cells specific for Mycobacterium tuberculosis were present in CCR6+CXCR3+ T helper type 1 subset. The elicitation of IL-17 responses correlated with the capacity of C. albicans hyphae to stimulate antigen-presenting cells for the priming of T(H)-17 responses in vitro and for the production of IL-23 but not IL-12. Our results demonstrate that human T(H)-17 cells have distinct migratory capacity and antigenic specificities and establish a link between microbial products, T helper cell differentiation and homing in response to fungal antigens.
Casey T Weaver - One of the best experts on this subject based on the ideXlab platform.
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γδ t cells recognize a microbial encoded b cell antigen to initiate a rapid antigen specific Interleukin 17 response
Immunity, 2012Co-Authors: Xun Zeng, Yu Ling Wei, Jun Huang, Evan W Newell, Brian A Kidd, Michael S Kuhns, Ray W Waters, Mark M Davis, Casey T WeaverAbstract:γδ T cells contribute uniquely to immune competence. Nevertheless, how they function remains an enigma. It is unclear what most γδ T cells recognize, what is required for them to mount an immune response, and how the γδ T cell response is integrated into host immune defense. Here, we report that a noted B cell antigen, the algae protein phycoerythrin (PE), is a murine and human γδ T cell antigen. Employing this specificity, we demonstrated that antigen recognition activated naive γδ T cells to make Interleukin-17 and respond to cytokine signals that perpetuate the response. High frequencies of antigen-specific γδ T cells in naive animals and their ability to mount effector response without extensive clonal expansion allow γδ T cells to initiate a swift, substantial response. These results underscore the adaptability of lymphocyte antigen receptors and suggest an antigen-driven rapid response in protective immunity prior to the maturation of classical adaptive immunity.
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Interleukin 17 producing cd4 effector t cells develop via a lineage distinct from the t helper type 1 and 2 lineages
Nature Immunology, 2005Co-Authors: Laurie E Harrington, Robin D Hatton, Paul R Mangan, Henrietta Turner, Theresa L Murphy, Kenneth M Murphy, Casey T WeaverAbstract:Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
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Interleukin 17 producing cd4 effector t cells develop via a lineage distinct from the t helper type 1 and 2 lineages
Nature Immunology, 2005Co-Authors: Laurie E Harrington, Robin D Hatton, Paul R Mangan, Henrietta Turner, Theresa L Murphy, Kenneth M Murphy, Casey T WeaverAbstract:CD4(+) T cells producing Interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (T(H)1) or T(H)2 lineages and instead favor the idea of a distinct effector lineage we call 'T(H)-17'. The development of T(H)-17 cells from naive precursor cells was potently inhibited by interferon-gamma (IFN-gamma) and IL-4, whereas committed T(H)-17 cells were resistant to suppression by T(H)1 or T(H)2 cytokines. In the absence of IFN-gamma and IL-4, IL-23 induced naive precursor cells to differentiate into T(H)-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-gamma signaling enhances development of pathogenic T(H)-17 effector cells that can exacerbate autoimmunity.
Antonio Lanzavecchia - One of the best experts on this subject based on the ideXlab platform.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of Interleukin 17–producing human T helper cells
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)-producing CD4(+) helper T cells (T(H)-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of T(H)-17 cells requires transforming growth factor-beta and IL-6 and the transcription factor RORgammat. We report here that for human naive CD4(+) T cells, RORgammat expression and T(H)-17 polarization were induced by IL-1beta and enhanced by IL-6 but were suppressed by transforming growth factor-beta and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced T(H)-17 priming, and this function correlated with antigen-presenting cell production of IL-1beta and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human T(H)-17 cells and emphasize an important difference in the requirements for the differentiation of T(H)-17 cells in humans and mice.
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Interleukins 1beta and 6 but not transforming growth factor beta are essential for the differentiation of Interleukin 17 producing human t helper cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Giorgio Napolitani, Antonio Lanzavecchia, Federica SallustoAbstract:Interleukin 17 (IL-17)–producing CD4+ helper T cells (TH-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of TH-17 cells requires transforming growth factor-β and IL-6 and the transcription factor RORγt. We report here that for human naive CD4+ T cells, RORγt expression and TH-17 polarization were induced by IL-1β and enhanced by IL-6 but were suppressed by transforming growth factor-β and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1β and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Surface phenotype and antigenic specificity of human Interleukin 17–producing T helper memory cells
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surface phenotype and antigenic specificity of human Interleukin 17 producing t helper memory cells
Nature Immunology, 2007Co-Authors: Eva V Acostarodriguez, Federica Sallusto, Antonio Lanzavecchia, Laura Rivino, Jens Geginat, David Jarrossay, Marco Gattorno, Giorgio NapolitaniAbstract:Interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) have been characterized in mice as a distinct subset of effector cells, but their identity and properties in humans remain elusive. We report here that expression of CCR6 and CCR4 together identified human memory CD4+ T cells selectively producing IL-17 and expressing mRNA encoding the human ortholog of mouse RORgammat, a transcription factor, whereas CCR6 and CXCR3 identified T(H)1 cells producing interferon-gamma and T helper cells producing both interferon-gamma and IL-17. Memory T cells specific for Candida albicans were present mainly in the CCR6+CCR4+ T(H)-17 subset, whereas memory T cells specific for Mycobacterium tuberculosis were present in CCR6+CXCR3+ T helper type 1 subset. The elicitation of IL-17 responses correlated with the capacity of C. albicans hyphae to stimulate antigen-presenting cells for the priming of T(H)-17 responses in vitro and for the production of IL-23 but not IL-12. Our results demonstrate that human T(H)-17 cells have distinct migratory capacity and antigenic specificities and establish a link between microbial products, T helper cell differentiation and homing in response to fungal antigens.