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Kylie M. Quinn Daniel E. Zak Andreia Costa Ayako Yamamoto Kathrin Kastenmuller Brenna J. Hill Geoffrey M. Lynn Patricia A. Darrah Ross W.B. Lindsay Lingshu Wang Cheng Cheng Alfredo Nicosia Antonella Folgori Stefano Colloca Riccardo Cortese Emma Gostick David A. Price Jason G.D. Gall Mario Roederer Alan Aderem Robert A. Seder 《The Journal of clinical investigation》2015,125(3):1129-1146
Recombinant adenoviral vectors (rAds) are lead vaccine candidates for protection against a variety of pathogens, including Ebola, HIV, tuberculosis, and malaria, due to their ability to potently induce T cell immunity in humans. However, the ability to induce protective cellular immunity varies among rAds. Here, we assessed the mechanisms that control the potency of CD8 T cell responses in murine models following vaccination with human-, chimpanzee-, and simian-derived rAds encoding SIV-Gag antigen (Ag). After rAd vaccination, we quantified Ag expression and performed expression profiling of innate immune response genes in the draining lymph node. Human-derived rAd5 and chimpanzee-derived chAd3 were the most potent rAds and induced high and persistent Ag expression with low innate gene activation, while less potent rAds induced less Ag expression and robustly induced innate immunity genes that were primarily associated with IFN signaling. Abrogation of type I IFN or stimulator of IFN genes (STING) signaling increased Ag expression and accelerated CD8 T cell response kinetics but did not alter memory responses or protection. These findings reveal that the magnitude of rAd-induced memory CD8 T cell immune responses correlates with Ag expression but is independent of IFN and STING and provide criteria for optimizing protective CD8 T cell immunity with rAd vaccines. 相似文献
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Durga Praveen Meka Anne Kathrin Müller-Rischart Prakash Nidadavolu Behnam Mohammadi Elisa Motori Srinivas Kumar Ponna Helia Aboutalebi Mahmoud Bassal Anil Annamneedi Barbara Finckh Margit Miesbauer Natalie Rotermund Christian Lohr J?rg Tatzelt Konstanze F. Winklhofer Edgar R. Kramer 《The Journal of clinical investigation》2015,125(5):1873-1885
Parkin and the glial cell line–derived neurotrophic factor (GDNF) receptor RET have both been independently linked to the dopaminergic neuron degeneration that underlies Parkinson’s disease (PD). In the present study, we demonstrate that there is genetic crosstalk between parkin and the receptor tyrosine kinase RET in two different mouse models of PD. Mice lacking both parkin and RET exhibited accelerated dopaminergic cell and axonal loss compared with parkin-deficient animals, which showed none, and RET-deficient mice, in which we found moderate degeneration. Transgenic expression of parkin protected the dopaminergic systems of aged RET-deficient mice. Downregulation of either parkin or RET in neuronal cells impaired mitochondrial function and morphology. Parkin expression restored mitochondrial function in GDNF/RET-deficient cells, while GDNF stimulation rescued mitochondrial defects in parkin-deficient cells. In both cases, improved mitochondrial function was the result of activation of the prosurvival NF-κB pathway, which was mediated by RET through the phosphoinositide-3-kinase (PI3K) pathway. Taken together, these observations indicate that parkin and the RET signaling cascade converge to control mitochondrial integrity and thereby properly maintain substantia nigra pars compacta dopaminergic neurons and their innervation in the striatum. The demonstration of crosstalk between parkin and RET highlights the interplay in the protein network that is altered in PD and suggests potential therapeutic targets and strategies to treat PD. 相似文献
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Kreitschmann-Andermahr Ilonka Siegel Sonja Unger Nicole Streetz-van der Werf Christine Karges Wolfram Schilbach Katharina Schröder Bernadette Szybowicz Janine Sauerwald Janina Zopf Kathrin Grzywotz Agnieszka Bidlingmaier Martin Sommer Heide Strasburger Christian J. 《Pituitary》2020,23(5):479-487
Pituitary - While reasons for non-adherence in children requiring growth hormone (GH) replacement (GH-Rx) are well researched, few studies have investigated adherence in adult GH deficient... 相似文献
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Heiko Sic Helene Kraus Josef Madl Karl-Andreas Flittner Audrey Lilly von Münchow Kathrin Pieper Marta Rizzi Anne-Kathrin Kienzler Korcan Ayata Sebastian Rauer Burkhard Kleuser Ulrich Salzer Meike Burger Katja Zirlik Vassilios Lougaris Alessandro Plebani Winfried Römer Christoph Loeffler Samantha Scaramuzza Anna Villa Emiko Noguchi Bodo Grimbacher Hermann Eibel 《The Journal of allergy and clinical immunology》2014
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Kathrin Pieper Marta Rizzi Matthaios Speletas Cristian R. Smulski Heiko Sic Helene Kraus Ulrich Salzer Gina J. Fiala Wolfgang W. Schamel Vassilios Lougaris Alessandro Plebani Lennart Hammarstrom Mike Recher Anastasios E. Germenis Bodo Grimbacher Klaus Warnatz Antonius G. Rolink Pascal Schneider Luigi D. Notarangelo Hermann Eibel 《The Journal of allergy and clinical immunology》2014
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Gijs Kooij Kathrin Kopplin Rosel Blasig Marchel Stuiver Nathalie Koning Gera Goverse Susanne M. A. van der Pol Bert van het Hof Maik Gollasch Joost A. R. Drexhage Arie Reijerkerk Iwan C. Meij Reina Mebius Thomas E. Willnow Dominik Müller Ingolf E. Blasig Helga E. de Vries 《Acta neuropathologica》2014,128(2):267-277
Multiple sclerosis (MS) is a chronic neuro-inflammatory disorder, which is marked by the invasion of the central nervous system by monocyte-derived macrophages and autoreactive T cells across the brain vasculature. Data from experimental animal models recently implied that the passage of leukocytes across the brain vasculature is preceded by their traversal across the blood–cerebrospinal fluid barrier (BCSFB) of the choroid plexus. The correlation between the presence of leukocytes in the CSF of patients suffering from MS and the number of inflammatory lesions as detected by magnetic resonance imaging suggests that inflammation at the choroid plexus contributes to the disease, although in a yet unknown fashion. We here provide first insights into the involvement of the choroid plexus in the onset and severity of the disease and in particular address the role of the tight junction protein claudin-3 (CLDN3) in this process. Detailed analysis of human post-mortem brain tissue revealed a selective loss of CLDN3 at the choroid plexus in MS patients compared to control tissues. Importantly, mice that lack CLDN3 have an impaired BCSFB and experience a more rapid onset and exacerbated clinical signs of experimental autoimmune encephalomyelitis, which coincides with enhanced levels of infiltrated leukocytes in their CSF. Together, this study highlights a profound role for the choroid plexus in the pathogenesis of multiple sclerosis, and implies that CLDN3 may be regarded as a crucial and novel determinant of BCSFB integrity. 相似文献
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B Sierra AB Pérez M Alvarez G García K Vogt E Aguirre K Schmolke HD Volk MG Guzmán 《The American journal of tropical medicine and hygiene》2012,87(3):538-547
Abstract. Secondary heterologous dengue infection is a risk factor for severe disease manifestations because of the immune-enhancement phenomenon. Succeeding clinical infections are seldom reported, and the clinical course of tertiary and quaternary dengue infections is not clear. Cuba represents a unique environment to study tertiary/quaternary dengue infections in a population with known clinical and serologic dengue markers and no dengue endemicity. We took advantage of this exceptional epidemiologic condition to study the effect of primary, secondary, tertiary, and quaternary dengue infection exposure on the expression of pro-inflammatory and regulatory cytokines, critical in dengue infection pathogenesis, by using a dengue infection ex vivo model. Whereas secondary exposure induced a high cytokine response, we found a significantly lower expression of tumor necrosis factor-α, interferon-γ, interleukin-10, and tumor growth factor-β after tertiary and quaternary infectious challenge. Significant differences in expression of the cytokines were seen between the dengue immune profiles, suggesting that the sequence in which the immune system encounters serotypes may be important in determining the nature of the immune response to subsequent infections. 相似文献