Monecke, Sebastian

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Tissue Antigens"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Hamann, Carina"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:38:32Z"],["dc.date.available","2018-11-07T09:38:32Z"],["dc.date.issued","2014"],["dc.format.extent","5"],["dc.identifier.isi","000337546000002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","1399-0039"],["dc.relation.issn","0001-2815"],["dc.title","PLURIPOTENT STEM CELLS VARYING IN A SINGLE MINOR HISTOCOMPATIBILITY ANTIGEN ELICIT CELLULAR AND HUMORAL IMMUNE RESPONSES THAT CAN MEDIATE GRAFT REJECTION"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","109"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Immunogenetics"],["dc.bibliographiccitation.lastpage","123"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Schilling, Daniela"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Multhoff, Gabriele"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T10:18:55Z"],["dc.date.available","2018-11-07T10:18:55Z"],["dc.date.issued","2016"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a ligand for the activating natural killer (NK) cell receptor NKG2D. A polymorphism causing a valine to methionine exchange at position 129 affects binding to NKG2D, cytotoxicity, interferon-gamma release by NK cells and activation of CD8(+) T cells. It is known that tumors can escape NKG2D-mediated immune surveillance by proteolytic shedding of MICA. Therefore, we investigated whether this polymorphism affects plasma membrane expression (pmMICA) and shedding of MICA. Expression of pmMICA was higher in a panel of tumor (n = 16, P = 0.0699) and melanoma cell lines (n = 13, P = 0.0429) carrying the MICA-129Val/Val genotype. MICA-129Val homozygous melanoma cell lines released more soluble MICA (sMICA) by shedding (P = 0.0015). MICA-129Met or MICA-129Val isoforms differing only in this amino acid were expressed in the MICA-negative melanoma cell line Malme, and clones with similar pmMICA expression intensity were selected. The MICA-129Met clones released more sMICA (P = 0.0006), and a higher proportion of the MICA-129Met than the MICA-129Val variant was retained in intracellular compartments (P = 0.0199). The MICA-129Met clones also expressed more MICA messenger RNA (P = 0.0047). The latter phenotype was also observed in mouse L cells transfected with the MICA expression constructs (P = 0.0212). In conclusion, the MICA-129Met/Val dimorphism affects the expression density of MICA on the plasma membrane. More of the MICA-129Met variants were retained intracellularly. If expressed at the cell surface, the MICA-129Met isoform was more susceptible to shedding. Both processes appear to limit the cell surface expression of MICA-129Met variants that have a high binding avidity to NKG2D."],["dc.identifier.doi","10.1007/s00251-015-0884-8"],["dc.identifier.isi","000369012800002"],["dc.identifier.pmid","26585323"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41550"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/128"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1432-1211"],["dc.relation.issn","0093-7711"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129Met/Val dimorphism affects plasma membrane expression and shedding of the NKG2D ligand MICA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1480"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1502"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Malzahn, Doerthe"],["dc.contributor.author","Viktorova, Elena"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Kilisch, Markus"],["dc.contributor.author","Wermuth, Janne Marieke"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Balavarca, Yesilda"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:49:36Z"],["dc.date.available","2018-11-07T09:49:36Z"],["dc.date.issued","2015"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a highly polymorphic ligand for the activating natural killer (NK)-cell receptor NKG2D. A single nucleotide polymorphism causes a valine to methionine exchange at position 129. Presence of a MICA-129Met allele in patients (n=452) undergoing hematopoietic stem cell transplantation (HSCT) increased the chance of overall survival (hazard ratio [HR]=0.77, P=0.0445) and reduced the risk to die due to acute graft-versus-host disease (aGVHD) (odds ratio [OR]=0.57, P=0.0400) although homozygous carriers had an increased risk to experience this complication (OR=1.92, P=0.0371). Overall survival of MICA-129Val/Val genotype carriers was improved when treated with anti-thymocyte globulin (HR=0.54, P=0.0166). Functionally, the MICA-129Met isoform was characterized by stronger NKG2D signaling, triggering more NK-cell cytotoxicity and interferon- release, and faster co-stimulation of CD8(+) T cells. The MICA-129Met variant also induced a faster and stronger down-regulation of NKG2D on NK and CD8(+) T cells than the MICA-129Val isoform. The reduced cell surface expression of NKG2D in response to engagement by MICA-129Met variants appeared to reduce the severity of aGVHD."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.15252/emmm.201505246"],["dc.identifier.isi","000364320100008"],["dc.identifier.pmid","26483398"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35542"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/127"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129 dimorphism affects NKG2D signaling and outcome of hematopoietic stem cell transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27300"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","27313"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Diederichs, Christopher"],["dc.contributor.author","Schill, Fabian"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Salinas, Gabriella"],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Pfister, Stefan"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Johnsen, Steven Arthur"],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2018-10-10T07:29:11Z"],["dc.date.available","2018-10-10T07:29:11Z"],["dc.date.issued","2017-04-18"],["dc.description.abstract","Pediatric high-grade gliomas (pedHGG) belong to the most aggressive cancers in children with a poor prognosis due to a lack of efficient therapeutic strategies. The β-catenin/Wnt-signaling pathway was shown to hold promising potential as a treatment target in adult high-grade gliomas by abrogating tumor cell invasion and the acquisition of stem cell-like characteristics. Since pedHGG differ from their adult counterparts in genetically and biologically we aimed to investigate the effects of β-catenin/Wnt-signaling pathway-inhibition by the β-catenin/CBP antagonist ICG-001 in pedHGG cell lines. In contrast to adult HGG, pedHGG cells displayed minimal detectable canonical Wnt-signaling activity. Nevertheless, low doses of ICG-001 inhibited cell migration/invasion, tumorsphere- and colony formation, proliferation in vitro as well as tumor growth in vivo/ovo, suggesting that ICG-001 affects pedHGG tumor cell characteristics independent of β-catenin/Wnt-signaling. RNA-sequencing analyses support a Wnt/β-catenin-independent effect of ICG-001 on target gene transcription, revealing strong effects on genes involved in cellular metabolic/biosynthetic processes and cell cycle progression. Among these, high mRNA expression of cell cycle regulator JDP2 was found to confer a better prognosis for pedHGG patients. In conclusion, ICG-001 might offer an effective treatment option for pedHGG patients functioning to regulate cell phenotype and gene expression programs in absence of Wnt/β-catenin signaling-activity."],["dc.fs.pkfprnr","86261"],["dc.identifier.doi","10.18632/oncotarget.15934"],["dc.identifier.fs","633047"],["dc.identifier.pmid","28460484"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14424"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15920"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The β-catenin/CBP-antagonist ICG-001 inhibits pediatric glioma tumorigenicity in a Wnt-independent manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","137"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","146"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Hueber, Daniela"],["dc.contributor.author","Geisler, Stephanie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2018-11-07T11:17:30Z"],["dc.date.available","2018-11-07T11:17:30Z"],["dc.date.issued","2008"],["dc.description.abstract","The outer dense fiber protein ODF2 is the major component of the sperm tall cytoskeleton and a critical component of the mature centriole of the centrosome. Centriole maturation involves the formation of appendages and the recruitment of ODF2/Cenexin. ODF2 and Cenexin are alternative splice variants that differ in a short stretch of amino acids at their N-terminal regions encoded by exon 3b. Whereas Cenexin is ubiquitously expressed, Odf2 is the predominant transcript of testes [Huber, D., Hoyer-Fender, S., 2007. Alternative splicing of exon 3b gives rise to ODF2 and Cenexin. Cytogenet. Genome Res. 119, doi: 10. 1159/000109621]. Here, we show that testicular expression of Odf2 correlates with spermiogenesis and ongoing sperm tail formation thus implicating functional differences between ODF2 and Cenexin. By generation of a series of ODF2/Cenexin deletion constructs fused to GFP and inspection of their subcellular localization in transfected NIH3T3 cells we found that a peptide of 42 amino acids specific for Cenexin is necessary for targeting ODF2/Cenexin to the centrosome and the primary cilium. Additionally, this region is also necessary for the formation of ODF2/Cenexin fibers that are associated with acetylated microtubules. Centrosomal targeting of ODF2/Cenexin does not depend on dynein-mediated transport further supporting an alternative targeting mechanism. However, part of the C-terminal coiled-coil region of ODF2 is also important in centrosomal/ciliary targeting and fiber formation presumably by supporting self-association and the formation of higher-order structures. (C) 2007 Elsevier GmbH. All rights reserved."],["dc.identifier.doi","10.1016/j.ejcb.2007.10.004"],["dc.identifier.isi","000254299300002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.relation.issn","0171-9335"],["dc.title","Molecular dissection of ODF2/Cenexin revealed a short stretch of amino acids necessary for targeting to the centrosome and the primary cilium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","104"],["dc.bibliographiccitation.journal","European Biophysics Journal"],["dc.bibliographiccitation.lastpage","105"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Doelker, N."],["dc.contributor.author","Blanchet, C."],["dc.contributor.author","Monecke, T."],["dc.contributor.author","Svergun, Dmitri I."],["dc.contributor.author","Ficner, Ralf"],["dc.contributor.author","Grubmüller, Helmut"],["dc.contributor.author","Dickmanns, A."],["dc.date.accessioned","2018-11-07T08:53:35Z"],["dc.date.available","2018-11-07T08:53:35Z"],["dc.date.issued","2011"],["dc.identifier.isi","000293637300233"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22448"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Budapest, HUNGARY"],["dc.relation.issn","0175-7571"],["dc.title","Allostery in nuclear export: a hybrid methods approach"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2665"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Röhrborn, Charlotte"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Reupke, Verena"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Lichtman, Andrew H."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:49:35Z"],["dc.date.available","2019-07-09T11:49:35Z"],["dc.date.issued","2018"],["dc.description.abstract","Heart failure due to pressure overload is frequently associated with inflammation. In addition to inflammatory responses of the innate immune system, autoimmune reactions of the adaptive immune system appear to be triggered in subgroups of patients with heart failure as demonstrated by the presence of autoantibodies against myocardial antigens. Moreover, T cell-deficient and T cell-depleted mice have been reported to be protected from heart failure induced by transverse aortic constriction (TAC) and we have shown recently that CD4+-helper T cells with specificity for an antigen in cardiomyocytes accelerate TAC-induced heart failure. In this study, we set out to investigate the potential contribution of CD8+-cytotoxic T cells with specificity to a model antigen (ovalbumin, OVA) in cardiomyocytes to pressure overload-induced heart failure. In 78% of cMy-mOVA mice with cardiomyocyte-specific OVA expression, a low-grade OVA-specific cellular cytotoxicity was detected after TAC. Adoptive transfer of OVA-specific CD8+-T cells from T cell receptor transgenic OT-I mice before TAC did not increase the risk of OVA-specific autoimmunity in cMy-mOVA mice. After TAC, again 78% of the mice displayed an OVA-specific cytotoxicity with on average only a three-fold higher killing of OVA-expressing target cells. More CD8+ cells were present after TAC in the myocardium of cMy-mOVA mice with OT-I T cells (on average 17.5/mm2) than in mice that did not receive OVA-specific CD8+-T cells (3.6/mm2). However, the extent of fibrosis was similar in both groups. Functionally, as determined by echocardiography, the adoptive transfer of OVA-specific CD8+-T cells did not significantly accelerate the progression from hypertrophy to heart failure in cMy-mOVA mice. These findings argue therefore against a major impact of cytotoxic T cells with specificity for autoantigens of cardiomyocytes in pressure overload-induced heart failure."],["dc.identifier.doi","10.3389/fimmu.2018.02665"],["dc.identifier.pmid","30498501"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15720"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59587"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/298"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","CD8+-T Cells With Specificity for a Model Antigen in Cardiomyocytes Can Become Activated After Transverse Aortic Constriction but Do Not Accelerate Progression to Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","0000-0003-1190-4040"],["cris.virtual.author-orcid","0000-0002-1651-1214"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.department","Institut für Pharmakologie und Toxikologie"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtualsource.author-orcid","bfb9620f-7265-426d-ad01-b0b69d13e6e5"],["cris.virtualsource.author-orcid","31870ba4-f58d-4096-b2fa-f1cead8d77c9"],["cris.virtualsource.author-orcid","d7d98060-8082-46e8-972f-2dfab1b501cc"],["cris.virtualsource.author-orcid","bf6f60ce-9405-4ab7-86c0-3ed9f441d244"],["cris.virtualsource.author-orcid","11b2f35d-3b48-45e1-b088-02271c68aaa1"],["cris.virtualsource.author-orcid","b88f3c2c-2563-4a4a-843e-a926abfe7876"],["cris.virtualsource.author-orcid","bb4ea395-7131-470f-8440-c9ba13eb663e"],["cris.virtualsource.author-orcid","b8e6502e-ec7d-43b8-89c1-27118d7c9bb2"],["cris.virtualsource.department","bfb9620f-7265-426d-ad01-b0b69d13e6e5"],["cris.virtualsource.department","31870ba4-f58d-4096-b2fa-f1cead8d77c9"],["cris.virtualsource.department","d7d98060-8082-46e8-972f-2dfab1b501cc"],["cris.virtualsource.department","bf6f60ce-9405-4ab7-86c0-3ed9f441d244"],["cris.virtualsource.department","11b2f35d-3b48-45e1-b088-02271c68aaa1"],["cris.virtualsource.department","b88f3c2c-2563-4a4a-843e-a926abfe7876"],["cris.virtualsource.department","bb4ea395-7131-470f-8440-c9ba13eb663e"],["cris.virtualsource.department","b8e6502e-ec7d-43b8-89c1-27118d7c9bb2"],["dc.bibliographiccitation.artnumber","924"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Johannsen, Hannah"],["dc.contributor.author","Muppala, Vijayakumar"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-04-23T11:49:21Z"],["dc.date.available","2018-04-23T11:49:21Z"],["dc.date.issued","2017"],["dc.description.abstract","The perspective to transplant grafts derived from pluripotent stem cells has gained much attention in recent years. Parthenogenetic stem cells (PSCs) are an alternative pluripotent stem cell type that is attractive as source of grafts for allogeneic transplantations because most PSCs are haploidentical for the major histocompatibility complex (MHC). This reduced immunogenetic complexity of PSCs could tremendously simplify the search for MHC-matched allogeneic stem cells. In this study, we have characterized immunological properties of the MHC haploidentical PSC line A3 (H2d/d) and the heterologous PSC line A6 (H2b/d). Both PSC lines largely lack MHC class I molecules, which present peptides to cytotoxic T lymphocytes (CTLs) and serve as ligands for inhibitory natural killer (NK) receptors. They express ligands for activating NK receptors, including the NKG2D ligand RAE-1, and the DNAM-1 ligands CD112 and CD155. Consequently, both PSC lines are highly susceptible to killing by IL-2-activated NK cells. In vitro-differentiated cells acquire resistance and downregulate ligands for activating NK receptors but fail to upregulate MHC class I molecules. The PSC line A6 and differentiated A6 cells are largely resistant to CTLs derived from T cell receptor transgenic OT-I mice after pulsing of the targets with the appropriate peptide. The high susceptibility to killing by activated NK cells may constitute a general feature of pluripotent stem cells as it has been also found with other pluripotent stem cell types. This activity potentially increases the safety of transplantations, if grafts contain traces of undifferentiated cells that could be tumorigenic in the recipient."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3389/fimmu.2017.00924"],["dc.identifier.gro","3142522"],["dc.identifier.pmid","28824647"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14593"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13678"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/213"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","1664-3224"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Immunological Properties of Murine Parthenogenetic Stem Cells and Their Differentiation Products"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","343"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","HLA"],["dc.bibliographiccitation.lastpage","344"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Huebscher, Daniela"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Hejazi, Maryam"],["dc.contributor.author","Uhrberg, Markus"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.date.accessioned","2018-11-07T10:23:29Z"],["dc.date.available","2018-11-07T10:23:29Z"],["dc.date.issued","2017"],["dc.identifier.isi","000400973300013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42464"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.publisher.place","Hoboken"],["dc.relation.issn","2059-2310"],["dc.relation.issn","2059-2302"],["dc.title","HUMAN CARDIOMYOCYTES DERIVED FROM INDUCED PLURIPOTENT STEM CELLS ARE TARGETS FOR ACTIVATED AUTOLOGOUS AND ALLOGENEIC NATURAL KILLER CELLS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","67"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Huebscher, Daniela"],["dc.contributor.author","Kaiser, Diana"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2018-11-07T10:27:34Z"],["dc.date.available","2018-11-07T10:27:34Z"],["dc.date.issued","2017"],["dc.description.abstract","Transplantation of stem cells represents an upcoming therapy for many degenerative diseases. For clinical use, transplantation of pluripotent stem cell-derived cells should lead to integration of functional grafts without immune rejection or teratoma formation. Our previous studies showed that the risk of teratoma formation is highly influenced by the immune system of the recipients. In this study, we have observed a higher teratoma formation rate when undifferentiated so-called multipotent adult germline stem cells (maGSCs) were transplanted into the heart of T, B, and natural killer (NK) cell-deficient RAG2(-/-)gamma c(-/-) mice than in RAG2(-/-) mice, which still have NK cells. Notably, in both strains, the teratoma formation rate was significantly reduced by the immunosuppressive drug cyclosporine A (CsA). Thus, CsA had a profound effect on teratoma formation independent of its immunosuppressive effects. The transplantation into RAG2(-/-) mice led to an activation of NK cells, which reached the maximum 14 days after transplantation and was not affected by CsA. The in vivo-activated NK cells efficiently killed YAC-1 and also maGSC target cells. This NK cell activation was confirmed in C57BL/6 wild-type mice whether treated with CsA or not. Sham operations in wild-type mice indicated that the inflammatory response to open heart surgery rather than the transplantation of maGSCs activated the NK cell system. An activation of NK cells during the transplantation of stem cell-derived in vitro differentiated grafts might be clinically beneficial by reducing the risk of teratoma formation by residual pluripotent cells."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3389/fimmu.2017.00067"],["dc.identifier.isi","000393436700001"],["dc.identifier.pmid","28220117"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14269"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43258"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/206"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1664-3224"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The Tumorigenicity of Multipotent Adult Germline Stem Cells Transplanted into the Heart Is Affected by Natural Killer Cells and by Cyclosporine A Independent of Its Immunosuppressive Effects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]