Brandt, Jens van den

[["dc.bibliographiccitation.firstpage","2384"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","American Journal of Transplantation"],["dc.bibliographiccitation.lastpage","2394"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Siepert, Anja"],["dc.contributor.author","Ahrlich, S."],["dc.contributor.author","Vogt, K."],["dc.contributor.author","Appelt, C."],["dc.contributor.author","Stanko, K."],["dc.contributor.author","Kühl, Anja A."],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Nizze, H."],["dc.contributor.author","Lehmann, M."],["dc.contributor.author","Tiedge, Markus"],["dc.contributor.author","Volk, H.-D."],["dc.contributor.author","Sawitzki, Birgit"],["dc.contributor.author","Reinke, Petra"],["dc.date.accessioned","2018-11-07T09:06:43Z"],["dc.date.available","2018-11-07T09:06:43Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent data suggest that donor-specific memory T cells (Tmem) are an independent risk factor for rejection and poor graft function in patients and a major challenge for immunosuppression minimizing strategies. Many tolerance induction protocols successfully proven in small animal models e.g. costimulatory blockade, T cell depletion failed in patients. Consequently, there is a need for more predictive transplant models to evaluate novel promising strategies, such as adoptive transfer of regulatory T cells (Treg). We established a clinically more relevant, life-supporting rat kidney transplant model using a high responder (DA to LEW) recipients that received donor-specific CD4+/ 8+ GFP+ Tmem before transplantation to achieve similar pre-transplant frequencies of donor-specific Tmem as seen in many patients. T cell depletion alone induced long-term graft survival in naive recipients but could not prevent acute rejection in Tmem+ rats, like in patients. Only if T cell depletion was combined with permanent CNI-treatment, the intragraft inflammation, and acute/chronic allograft rejection could be controlled long-term. Remarkably, combining 10 days CNI treatment and adoptive transfer of Tregs (day 3) but not Treg alone also induced long-term graft survival and an intragraft tolerance profile (e.g. high TOAG-1) in Tmem+ rats. Our model allows evaluation of novel therapies under clinically relevant conditions."],["dc.identifier.doi","10.1111/j.1600-6143.2012.04143.x"],["dc.identifier.isi","000307945000017"],["dc.identifier.pmid","22702307"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25617"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1600-6135"],["dc.title","Permanent CNI Treatment for Prevention of Renal Allograft Rejection in Sensitized Hosts Can Be Replaced by Regulatory T Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Immunology"],["dc.bibliographiccitation.lastpage","53"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Lim, Hee-Young"],["dc.contributor.author","Mueller, Nora"],["dc.contributor.author","Herold, Marco J."],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:59:00Z"],["dc.date.available","2018-11-07T10:59:00Z"],["dc.date.issued","2007"],["dc.description.abstract","Glucocorticoids (GCs) are involved in the modulation of macrophage function and thereby control the host's immune responses to pathogens. However, neither the role of hormone concentration nor the differential contribution of the glucocorticoid (GR) and the mineralocorticoid receptors (MR) to these activities are known. Here we show that low levels of corticosterone enhance NO production as well as mRNA expression of pro-inflammatory cytokines, chemokines and enzymes required for mediator synthesis. In contrast, at high corticosterone concentrations macrophage function was strongly repressed. Importantly, inactivation of the GR by lentiviral delivery of siRNAs abrogated both the immunostimulatory and the immunosuppressive GC actions whereas inactivation of the MR had no effect. Furthermore, removal of endogenous GCs by adrenalectomy in vivo induced a preactivated state in macrophages that could be modulated by corticosterone. We conclude that GCs exert distinct effects on macrophage function dependent on their concentration, and that they primarily act through the GR despite concomitant expression of the MR."],["dc.identifier.doi","10.1111/j.1365-2567.2007.02611.x"],["dc.identifier.isi","000249040700005"],["dc.identifier.pmid","17451463"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50596"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0019-2805"],["dc.title","Glucocorticoids exert opposing effects on macrophage function dependent on their concentration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger"],["dc.contributor.author","Kitz, Alexandra"],["dc.contributor.author","Nosov, Michail"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:02:16Z"],["dc.date.available","2018-11-07T09:02:16Z"],["dc.date.issued","2012"],["dc.identifier.isi","000312764800352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Boston, MA"],["dc.title","Direct imaging of T cell activation during experimental autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","17"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","27"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Camara, Monika"],["dc.contributor.author","Beyersdorf, Niklas"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Herold, Marco J."],["dc.contributor.author","Ip, Chi Wang"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Taurog, Joel D."],["dc.contributor.author","Huenig, Thomas"],["dc.contributor.author","Herrmann, Thomas R."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Weishaupt, Andreas"],["dc.contributor.author","Kerkau, Thomas"],["dc.date.accessioned","2018-11-07T09:22:23Z"],["dc.date.available","2018-11-07T09:22:23Z"],["dc.date.issued","2013"],["dc.description.abstract","The role of CD8(+) T cells in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is still unclear. We describe here significantly reduced disease activity of EAE both in Lewis rats, depleted of CD8(+) T cells by monoclonal antibodies and CD8 knockout rats, which was accompanied by reduced leukocyte infiltration into the spinal cord. We detected myelin basic protein (MBP)-specific CD4(+) T cells in peripheral lymphoid organs of CD8-depleted animals which, however, failed to differentiate into interferon-gamma-producing effector cells. Our results indicate that CD8(+) T cells interact with myelin-specific CD4(+) T cells early in EAE enabling them to differentiate into pathogenic effector cells. (C) 2013 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2013.04.014"],["dc.identifier.isi","000321093000003"],["dc.identifier.pmid","23664330"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29330"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","CD8(+) T cell help is required for efficient induction of EAE in Lewis rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Wiener klinische Wochenschrift"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Wuest, S."],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Reichardt, M."],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T11:12:50Z"],["dc.date.available","2018-11-07T11:12:50Z"],["dc.date.issued","2008"],["dc.format.extent","52"],["dc.identifier.isi","000259367100164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53751"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0043-5325"],["dc.title","Peripheral T cells are the therapeutic targets of high-dose glucocorticoids in experimental autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","American Journal of Transplantation"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Siepert, Anja"],["dc.contributor.author","Sawitzki, Birgit"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Nizze, Horst"],["dc.contributor.author","Tiedge, Markus"],["dc.contributor.author","Lehmann, Manfred"],["dc.contributor.author","Volk, Hans D."],["dc.contributor.author","Reinke, Petra"],["dc.date.accessioned","2018-11-07T08:46:55Z"],["dc.date.available","2018-11-07T08:46:55Z"],["dc.date.issued","2010"],["dc.format.extent","22"],["dc.identifier.isi","000273654600083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20812"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","American-Society-of-Transplantation Annual Scientific Exchange"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1600-6135"],["dc.title","Synergistic Effect of CsA and Tregs in Preventing Memory T Cell Induced Tolerance Abrogation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","32"],["dc.bibliographiccitation.volume","290"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Lingner, Thomas"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Weishaupt, Andreas"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:19:23Z"],["dc.date.available","2018-11-07T10:19:23Z"],["dc.date.issued","2016"],["dc.description.abstract","MS is a highly prevalent neuroinflammatory disease of presumed autoimmune origin. Clinical observations and animal studies suggest that CD8(+) T cells play an important role in MS but their exact mechanisms are ill defined. When we actively induced EAE in CD8 knock-out DA rats, or adoptively transferred encephalitogenic CD4(+) T cells into CD8 knock-out DA rats, the disease course was indistinguishable from controls. Since our previous findings had revealed that the absence of CD8(+) T cells in Lewis rats ameliorated EAE, we compared antigen-induced T cell differentiation in both strains. Disease onset and the composition of the draining lymph nodes were similar but T cell activation in DA rats was much weaker. Moreover, oligoclonal expansion of CD8(+) T cells was exclusively observed in Lewis but not in DA rats. This suggests that myelin-specific CD8(+) T cells are involved in the differentiation of encephalitogenic CD4(+) T cells in Lewis rats, whilst they do not impact CD4(+) T cell priming in DA rats. Hence, clonal expansion of CD8(+) T cells in secondary lymphoid organs appears to be linked to their ability to modulate CNS autoimmune responses. (C) 2015 Published by Elsevier B.V."],["dc.description.sponsorship","German Research Foundation (DFG) [SFB/TRR 43]"],["dc.identifier.doi","10.1016/j.jneuroim.2015.10.020"],["dc.identifier.isi","000368955000005"],["dc.identifier.pmid","26711565"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41645"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Modulation of CNS autoimmune responses by CD8(+) T cells coincides with their oligoclonal expansion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1304"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Molecular Endocrinology"],["dc.bibliographiccitation.lastpage","1311"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Lim, Hee-Young"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Fassnacht, Martin"],["dc.contributor.author","Allolio, Bruno"],["dc.contributor.author","Herold, Marco J."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T11:14:48Z"],["dc.date.available","2018-11-07T11:14:48Z"],["dc.date.issued","2008"],["dc.description.abstract","Currently, gene disruption by homologous recombination in embryonic stem cells is only feasible in mice. To circumvent this problem, we silenced mineralocorticoid receptor (MR) expression by RNA interference in knockdown rats generated through lentiviral transgenesis. Analysis of the F1 progeny at 3 wk of age revealed strongly decreased MR levels. This was specific for the targeted gene and related to the abundance of the short interfering RNA. Reminiscent of MR knockout mice, the transgenic rats showed a reduced body weight, elevated serum aldosterone levels, increased plasma renin activity, and altered expression of MR target genes. Some of these effects correlated with the degree to which MR mRNA expression was reduced. Whereas disruption of the MR by gene targeting in mice leads to postnatal death, our strategy also allowed obtaining adult knockdown rats with defects in hormone and electrolyte homeostasis resembling pseudohypoaldosteronism. In conclusion, this is the first example of a human disease model based on RNA interference in rats."],["dc.identifier.doi","10.1210/me.2007-0417"],["dc.identifier.isi","000256307800002"],["dc.identifier.pmid","18337591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54223"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0888-8809"],["dc.title","Silencing of the mineralocorticoid receptor by ribonucleic acid interference in transgenic rats disrupts endocrine homeostasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1041"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","1053"],["dc.bibliographiccitation.volume","170"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","McPherson, Kirsty G."],["dc.contributor.author","de Graaf, Katrien L."],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Wiehr, Stefan"],["dc.contributor.author","Herrmann, Thomas R."],["dc.contributor.author","Weissert, Robert"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T11:04:12Z"],["dc.date.available","2018-11-07T11:04:12Z"],["dc.date.issued","2007"],["dc.description.abstract","To study the effect of enhanced glucocorticoid signaling on T cells, we generated transgenic rats overexpressmig a mutant glucocorticoid receptor with increased ligand affinity in the thymus. We found that this caused massive thymocyte apoptosis at physiological hormone levels, which could be reversed by adrenalectomy. Due to homeostatic proliferation, a considerable number of mature T lymphocytes accumulated in the periphery, responding normally to costimulation but exhibiting a perturbed T-cell repertoire. Furthermore, the transgenic rats showed increased resistance to experimental autoimmune encephalomyelitis, which manifests in a delayed onset and milder disease course, impaired leukocyte infiltration into the central nervous system and a distinct cytokine profile. in contrast, the ability of the transgenic rats to mount an allergic airway response to ovalbumin was not compromised, although isotype switching of antigen-specific immunoglobulins was altered. Collectively, our findings suggest that endogenous glucocorticoids impact T-cell development and favor the selection of Th2- over TH1-dominated adaptive immune responses."],["dc.identifier.doi","10.2353/ajpath.2007.060804"],["dc.identifier.isi","000244574500024"],["dc.identifier.pmid","17322387"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51781"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.title","Enhanced glucocorticoid receptor signaling in T cells impacts thymocyte apoptosis and adaptive immune responses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1326"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","1338"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Lingner, Thomas"],["dc.contributor.author","Bommhardt, Ursula"],["dc.contributor.author","Sendtner, Michael"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T09:57:51Z"],["dc.date.available","2018-11-07T09:57:51Z"],["dc.date.issued","2015"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) promotes neuronal survival, regeneration, and plasticity. Emerging evidence also indicates an essential role for BDNF outside the nervous system, for instance in immune cells. We therefore investigated the impact of BDNF on Tcells using BDNF knockout (KO) mice and conditional KO mice lacking BDNF specifically in this lymphoid subset. In both settings, we observed diminished T-cell cellularity in peripheral lymphoid organs and an increase in CD4(+)CD44(+) memory Tcells. Analysis of thymocyte development revealed diminished total thymocyte numbers, accompanied by a significant increase in CD4/CD8 double-negative (DN) thymocytes due to a partial block in the transition from the DN3 to the DN4 stage. This was neither due to increased thymocyte apoptosis nor defects in the expression of the TCR- chain or the pre-TCR. In contrast, pERK but not pAKT levels were diminished in DN3 BDNF-deficient thymocytes. BDNF deficiency in Tcells did not result in gross deficits in peripheral acute immune responses nor in changes of the homeostatic proliferation of peripheral Tcells. Taken together, our data reveal a critical autocrine and/or paracrine role of T-cell-derived BDNF in thymocyte maturation involving ERK-mediated TCR signaling pathways."],["dc.identifier.doi","10.1002/eji.201444985"],["dc.identifier.isi","000354182300006"],["dc.identifier.pmid","25627579"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37248"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.title","Thymocyte-derived BDNF influences T-cell maturation at the DN3/DN4 transition stage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]