Reichardt, Holger Michael

[["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","48"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","61"],["dc.bibliographiccitation.volume","199"],["dc.contributor.author","Klaßen, Carina"],["dc.contributor.author","Karabinskaya, Anna"],["dc.contributor.author","Dejager, Lien"],["dc.contributor.author","Vettorazzi, Sabine"],["dc.contributor.author","Van Moorleghem, Justine"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Meijsing, Sebastiaan H."],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Libert, Claude"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2020-12-10T18:47:42Z"],["dc.date.available","2020-12-10T18:47:42Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.4049/jimmunol.1601691"],["dc.identifier.eissn","1550-6606"],["dc.identifier.issn","0022-1767"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78852"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Wiener klinische Wochenschrift"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Mueller, N."],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T11:12:50Z"],["dc.date.available","2018-11-07T11:12:50Z"],["dc.date.issued","2008"],["dc.format.extent","63"],["dc.identifier.isi","000259367100198"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53752"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0043-5325"],["dc.title","Repression of T effector cells by glucocorticoids through rapid modulation of the F-actin cytoskeleton by non-genomic mechanisms"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1127"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Annals of Hematology"],["dc.bibliographiccitation.lastpage","1133"],["dc.bibliographiccitation.volume","96"],["dc.contributor.author","Budde, Holger"],["dc.contributor.author","Papert, Susanne"],["dc.contributor.author","Maas, Jens-Holger"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Legler, Tobias Joerg"],["dc.date.accessioned","2018-11-07T10:22:22Z"],["dc.date.available","2018-11-07T10:22:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Graft-versus-host disease (GvHD) still belongs to the major challenges after allogeneic hematopoietic stem cell transplantation (HSCT). Immune-suppressive therapy against GvHD is a double-edged sword due to risk of infections and relapse. The ability to adapt prophylactic treatment according to the probability of severe GvHD would be an essential advantage for the patients. We analyzed different biomarkers for their potential to predict the development of GvHD in 28 patients who underwent allogeneic HSCT. Blood was taken once directly after hematopoietic engraftment. In this study, patients were monitored for 12 months after HSCT for the occurrence of acute GvHD or acute/chronic GvHD overlap syndrome. Soluble IL-2 receptor and CD4/CD8 T cell ratio were independently associated with the occurrence of GvHD in the observation period. However, the largest area under the receiver operating characteristic curve with 0.90 was observed when a 5-parameter biomarker score based on CD4(+) T cells, CD8(+) T cells, CD19(-) CD21(+) precursor B cells, CD4/CD8 T cell ratio, and soluble IL-2 receptor was used to predict GvHD. In addition, CD8(+) T cell levels above 2.3% of all mononuclear cells after engraftment may predict relapse-free survival at least for 12 months. In summary, we found a new biomarker panel for prediction of GvHD which is featured by established laboratory assays and high statistical significance. In order to introduce the biomarker panel into routine clinical protocols, we suggest performing a larger multi-center study."],["dc.identifier.doi","10.1007/s00277-017-2999-5"],["dc.identifier.isi","000403078900008"],["dc.identifier.pmid","28447161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42255"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0584"],["dc.relation.issn","0939-5555"],["dc.title","Prediction of graft-versus-host disease: a biomarker panel based on lymphocytes and cytokines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Endocrine Reviews"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Furlow, J. David"],["dc.contributor.author","Watson, Monica L."],["dc.contributor.author","Baehr, Leslie M."],["dc.contributor.author","Karbassi, E."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Bodine, Sue C."],["dc.date.accessioned","2018-11-07T08:42:33Z"],["dc.date.available","2018-11-07T08:42:33Z"],["dc.date.issued","2010"],["dc.identifier.isi","000281989401038"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19726"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.publisher.place","Chevy chase"],["dc.relation.conference","92nd Meeting and Expo of the Endocrine Society (ENDO 2010)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","0163-769X"],["dc.title","The Glucocorticoid Receptor and Its Direct Target Gene MuRF1 Are Required for Dexamethasone-Induced Skeletal Muscle Atrophy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Infection"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Kleiman, Anna"],["dc.contributor.author","Huebner, S."],["dc.contributor.author","Heuer, H."],["dc.contributor.author","Winning, J."],["dc.contributor.author","Berger, S."],["dc.contributor.author","Libert, Claude"],["dc.contributor.author","Weigand, Markus A."],["dc.contributor.author","Schuetz, Guenther"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Bauer, M."],["dc.contributor.author","Tuckermann, Jan P."],["dc.date.accessioned","2018-11-07T08:52:27Z"],["dc.date.available","2018-11-07T08:52:27Z"],["dc.date.issued","2011"],["dc.format.extent","S109"],["dc.identifier.isi","000294888800036"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22165"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0300-8126"],["dc.title","Glucocorticoids control systemic inflammatory response by regulation of energy metabolism and cytokine expression"],["dc.type","conference_abstract"],["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.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Rocamora-Reverte, Lourdes"],["dc.contributor.author","Tuzlak, Selma"],["dc.contributor.author","von Raffay, Laura"],["dc.contributor.author","Tisch, Marcel"],["dc.contributor.author","Fiegl, Heidi"],["dc.contributor.author","Drach, Mathias"],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Villunger, Andreas"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Wiegers, G. Jan"],["dc.date.accessioned","2020-12-10T18:44:25Z"],["dc.date.available","2020-12-10T18:44:25Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3389/fimmu.2019.00472"],["dc.identifier.eissn","1664-3224"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78442"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Glucocorticoid Receptor-Deficient Foxp3+ Regulatory T Cells Fail to Control Experimental Inflammatory Bowel Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1083"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Boutin, Philippe"],["dc.contributor.author","Neumann, Konstantin"],["dc.contributor.author","Bremes, Vanessa"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Waetzig, Vicky"],["dc.contributor.author","Herdegen, Thomas"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Greig, Iain"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:56:53Z"],["dc.date.available","2018-11-07T09:56:53Z"],["dc.date.issued","2015"],["dc.description.abstract","The putative protein tyrosine kinase (PTK) inhibitor tyrphostin AG126 has proven beneficial in various models of inflammatory disease. Yet molecular targets and cellular mechanisms remained enigmatic. We demonstrate here that AG126 treatment has beneficial effects in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. AG126 alleviates the clinical symptoms, diminishes encephalitogenic Th17 differentiation, reduces inflammatory CNS infiltration as well as microglia activation and attenuates myelin damage. We show that AG126 directly inhibits Bruton's tyrosine kinase (BTK), a PTK associated with B cell receptor and Toll-like receptor (TLR) signaling. However, BTK inhibition cannot account for the entire activity spectrum. Effects on TLR-induced proinflammatory cytokine expression in microglia involve AG126 hydrolysis and conversion of its dinitrile side chain to malononitrile (MN). Notably, while liberated MN can subsequently mediate critical AG126 features, full protection in EAE still requires delivery of intact AG126. Its anti-inflammatory potential and especially interference with TLR signaling thus rely on a dual mechanism encompassing BTK and a novel MN-sensitive target. Both principles bear great potential for the therapeutic management of disturbed innate and adaptive immune functions. GLIA 2015;63:1083-1099"],["dc.identifier.doi","10.1002/glia.22803"],["dc.identifier.isi","000353244400011"],["dc.identifier.pmid","25731696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Tyrphostin AG126 Exerts Neuroprotection in CNS Inflammation by a Dual Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","24"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","ChemNanoMat"],["dc.bibliographiccitation.lastpage","45"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Neumeier, B. Lilli"],["dc.contributor.author","Khorenko, Mikhail"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Goldmann, Oliver"],["dc.contributor.author","Napp, Joanna"],["dc.contributor.author","Schepers, Ute"],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Feldmann, Claus"],["dc.date.accessioned","2022-03-01T11:45:18Z"],["dc.date.available","2022-03-01T11:45:18Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/cnma.201800310"],["dc.identifier.issn","2199-692X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103282"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","2199-692X"],["dc.title","Fluorescent Inorganic-Organic Hybrid Nanoparticles"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]