Gröschel, Carina

[["dc.bibliographiccitation.firstpage","1272"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.lastpage","1278"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Gröschel, S."],["dc.contributor.author","Lange, B."],["dc.contributor.author","Grond, M."],["dc.contributor.author","Jauss, M."],["dc.contributor.author","Kirchhof, P."],["dc.contributor.author","Rostock, T."],["dc.contributor.author","Wachter, R."],["dc.contributor.author","Gröschel, K."],["dc.contributor.author","Uphaus, T."],["dc.date.accessioned","2021-04-14T08:26:36Z"],["dc.date.available","2021-04-14T08:26:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1111/ene.14250"],["dc.identifier.eissn","1468-1331"],["dc.identifier.issn","1351-5101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82012"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1468-1331"],["dc.relation.issn","1351-5101"],["dc.title","Automatic Holter electrocardiogram analysis in ischaemic stroke patients to detect paroxysmal atrial fibrillation: ready to replace physicians?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1311"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Amino Acids"],["dc.bibliographiccitation.lastpage","1312"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Roviello, G."],["dc.contributor.author","Gröschel, S."],["dc.contributor.author","Pedone, C."],["dc.contributor.author","Diederichsen, U."],["dc.date.accessioned","2011-07-21T15:09:45Z"],["dc.date.accessioned","2021-10-27T13:12:09Z"],["dc.date.available","2011-07-21T15:09:45Z"],["dc.date.available","2021-10-27T13:12:09Z"],["dc.date.issued","2010"],["dc.format.mimetype","application/pdf"],["dc.identifier.doi","10.1007/s00726-009-0455-0"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6770"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91664"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.publisher","Springer Vienna"],["dc.publisher.place","Vienna"],["dc.relation.eissn","1438-2199"],["dc.relation.iserratumof","/handle/2/19939"],["dc.relation.issn","0939-4451"],["dc.relation.orgunit","Fakultät für Chemie"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","540"],["dc.title","Erratum to: Synthesis of novel MMT/acyl-protected nucleo alanine monomers for the preparation of DNA/alanyl-PNA chimeras"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","erratum_ja"],["dc.type.version","published_version"],["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"]]

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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.artnumber","15998"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Röhrborn, Charlotte"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Kruse, Vanessa"],["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","Dressel, Ralf"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-04-23T11:49:16Z"],["dc.date.available","2018-04-23T11:49:16Z"],["dc.date.issued","2017"],["dc.description.abstract","We investigated whether CD4+-T cells with specificity for an antigen in cardiomyocytes promote the progression from hypertrophy to heart failure in mice with increased pressure load due to transverse aortic constriction (TAC). OT-II mice expressing a transgenic T cell receptor (TCR) with specificity for ovalbumin (OVA) on CD4+-T cells and cMy-mOVA mice expressing OVA on cardiomyocytes were crossed. The resulting cMy-mOVA-OT-II mice did not display signs of spontaneous autoimmunity despite the fact that their OVA-specific CD4+-T cells were not anergic. After TAC, progression to heart failure was significantly accelerated in cMy-mOVA-OT-II compared to cMy-mOVA mice. No OVA-specific antibodies were induced in response to TAC in cMy-mOVA-OT-II mice, yet more CD3+ T cells infiltrated their myocardium when compared with TAC-operated cMy-mOVA mice. Systemically, the proportion of activated CD4+-T cells with a Th1 and Th17 cytokine profile was increased in cMy-mOVA-OT-II mice after TAC. Thus, T helper cells with specificity for an antigen in cardiomyocytes can directly promote the progression of heart failure in response to pressure overload independently of autoantibodies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1038/s41598-017-16147-1"],["dc.identifier.gro","3142514"],["dc.identifier.pmid","29167489"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13669"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/196"],["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 | 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.issn","2045-2322"],["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.title","T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure"],["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.artnumber","870"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Polić, Bojan"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:43:35Z"],["dc.date.available","2019-07-09T11:43:35Z"],["dc.date.issued","2017"],["dc.description.abstract","Natural killer (NK) cells play an important role as cytotoxic effector cells, which scan the organism for infected or tumorigenic cells. Conflicting data have been published whether NK cells can also kill allogeneic or even autologous pluripotent stem cells (PSCs) and which receptors are involved. A clarification of this question is relevant since an activity of NK cells against PSCs could reduce the risk of teratoma growth after transplantation of PSC-derived grafts. Therefore, the hypothesis has been tested that the activity of NK cells against PSCs depends on cytokine activation and specifically on the activating NK receptor NKG2D. It is shown that a subcutaneous injection of autologous iPSCs failed to activate NK cells against these iPSCs and can give rise to teratomas. In agreement with this result, several PSC lines, including two iPSC, two embryonic stem cell (ESC), and two so-called multipotent adult germline stem cell (maGSC) lines, were largely resistant against resting NK cells although differences in killing were found at low level. All PSC lines were killed by interleukin (IL)-2-activated NK cells, and maGSCs were better killed than the other PSC types. The PSCs expressed ligands of the activating NK receptor NKG2D and NKG2D-deficient NK cells from Klrk1−/− mice were impaired in their cytotoxic activity against PSCs. The low-cytotoxic activity of resting NK cells was almost completely dependent on NKG2D. The cytotoxic activity of IL-2-activated NKG2D-deficient NK cells against PSCs was reduced, indicating that also other activating receptors on cytokine-activated NK cells must be engaged by ligands on PSCs. Thus, NKG2D is an important activating receptor involved in killing of murine PSCs. However, NK cells need to be activated by cytokines before they efficiently target PSCs and then also other NK receptors become relevant. These features of NK cells might be relevant for transplantation of PSC-derived grafts since NK cells have the capability to kill undifferentiated cells, which might be present in grafts in trace amounts."],["dc.identifier.doi","10.3389/fimmu.2017.00870"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14587"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58923"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/297"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["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.eissn","1664-3224"],["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.subject.ddc","610"],["dc.title","Efficient Killing of Murine Pluripotent Stem Cells by Natural Killer (NK) Cells Requires Activation by Cytokines and Partly Depends on the Activating NK Receptor NKG2D"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]