Dressel, Ralf

[["dc.bibliographiccitation.journal","Wiener klinische Wochenschrift"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Novota, P."],["dc.contributor.author","Sviland, Lisbet"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Hitt, Reiner"],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Walter, L."],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T11:12:51Z"],["dc.date.available","2018-11-07T11:12:51Z"],["dc.date.issued","2008"],["dc.format.extent","124"],["dc.identifier.isi","000259367100404"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53754"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0043-5325"],["dc.title","Major histocompatibility complex (MHC) gene expression profiling of the graft versus host reaction in skin explant assays"],["dc.type","conference_abstract"],["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","9"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Greinix, Hildegard T."],["dc.contributor.author","Holler, Ernst"],["dc.contributor.author","Dickinson, Anne M."],["dc.date.accessioned","2020-12-10T18:44:24Z"],["dc.date.available","2020-12-10T18:44:24Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3389/fimmu.2018.01966"],["dc.identifier.eissn","1664-3224"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78441"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Editorial: Cellular Therapies: Past, Present and Future"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","editorial_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","322"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Tissue Antigens"],["dc.bibliographiccitation.lastpage","323"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Novota, P."],["dc.contributor.author","Sviland, Lisbet"],["dc.contributor.author","Wang, X. N."],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T11:16:59Z"],["dc.date.available","2018-11-07T11:16:59Z"],["dc.date.issued","2008"],["dc.identifier.isi","000254629500154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54710"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","22nd European Immunogenetics and Histocompatibility Conference"],["dc.relation.eventlocation","Toulouse, FRANCE"],["dc.relation.issn","0001-2815"],["dc.title","The expression of the Hsp 70-1 and Hsp 70-2 genes correlates with the degree of graft-versus-host reaction in a rat skin explant model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","380"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Gam, Rihab"],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Crossland, Rachel E."],["dc.contributor.author","Norden, Jean"],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:43:18Z"],["dc.date.available","2019-07-09T11:43:18Z"],["dc.date.issued","2017"],["dc.description.abstract","The outcome of hematopoietic stem cell transplantation (HSCT) is controlled by genetic factors among which the leukocyte antigen human leukocyte antigen (HLA) matching is most important. In addition, minor histocompatibility antigens and non-HLA gene polymorphisms in genes controlling immune responses are known to contribute to the risks associated with HSCT. Besides single-nucleotide polymorphisms (SNPs) in protein coding genes, SNPs in regulatory elements such as microRNAs (miRNAs) contribute to these genetic risks. However, genetic risks require for their realization the expression of the respective gene or miRNA. Thus, gene and miRNA expression studies may help to identify genes and SNPs that indeed affect the outcome of HSCT. In this review, we summarize gene expression profiling studies that were performed in recent years in both patients and animal models to identify genes regulated during HSCT. We discuss SNP– mRNA–miRNA regulatory networks and their contribution to the risks associated with HSCT in specific examples, including forkheadbox protein 3 and regulatory T cells, the role of the miR-155 and miR-146a regulatory network for graft-versus-host disease, and the function of MICA and its receptor NKG2D for the outcome of HSCT. These examples demonstrate how SNPs affect expression or function of proteins that modulate the alloimmune response and influence the outcome of HSCT. Specific miRNAs targeting these genes and directly affecting expression of mRNAs are identified. It might be valuable in the future to determine SNPs and to analyze miRNA and mRNA expression in parallel in cohorts of HSCT patients to further elucidate genetic risks of HSCT."],["dc.identifier.doi","10.3389/fimmu.2017.00380"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14421"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58858"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/315963/EU/Improving HSCT By Validation Of Biomarkers & Development Of Novel Cellular Therapies/CELLEUROPE"],["dc.relation.issn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genetic Association of Hematopoietic Stem Cell Transplantation Outcome beyond Histocompatibility Genes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S20"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","S21"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Gam, R."],["dc.contributor.author","Norden, J."],["dc.contributor.author","Crossland, Rachel E."],["dc.contributor.author","Pearce, Kim F."],["dc.contributor.author","Holler, Ernst"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Dickinson, Anne M."],["dc.date.accessioned","2018-11-07T10:00:09Z"],["dc.date.available","2018-11-07T10:00:09Z"],["dc.date.issued","2015"],["dc.identifier.isi","000351632900034"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37741"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","London"],["dc.relation.conference","41st Annual Meeting of the European-Society-for-Blood-and-Marrow-Transplantation"],["dc.relation.eventlocation","Istanbul, TURKEY"],["dc.relation.issn","1476-5365"],["dc.relation.issn","0268-3369"],["dc.title","MICA genotype, serum and expression level effects on the outcome of HSCT"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","404"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","International Journal of Immunogenetics"],["dc.bibliographiccitation.lastpage","412"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Pearce, Kim F."],["dc.contributor.author","Balavarca, Yesilda"],["dc.contributor.author","Norden, J."],["dc.contributor.author","Jackson, Graham H."],["dc.contributor.author","Holler, Ernst"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Greinix, Hildegard T."],["dc.contributor.author","Toubert, A."],["dc.contributor.author","Gluckman, E."],["dc.contributor.author","Hromadnikova, Ilona"],["dc.contributor.author","Sedlacek, Petr"],["dc.contributor.author","Wolff, Daniel"],["dc.contributor.author","Holtick, U."],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Dickinson, Anne M."],["dc.date.accessioned","2018-11-07T10:04:45Z"],["dc.date.available","2018-11-07T10:04:45Z"],["dc.date.issued","2016"],["dc.description.abstract","The EBMT risk score is an established tool successfully used in the prognosis of survival post-HSCT and is applicable for a range of haematological disorders. One of its main advantages is that score generation involves summation of clinical parameters that are available pretransplant. However, the EBMT risk score is recognized as not being optimal. Previous analyses, involving patients with various diagnoses, have shown that non-HLA gene polymorphisms influence outcome after allogeneic HSCT. This study is novel as it focuses only on patients having acute leukaemia (N = 458) and attempts to demonstrate how non-HLA gene polymorphisms can be added to the EBMT risk score in a Cox regression model to improve prognostic ability for overall survival. The results of the study found that three genetic factors improved EBMT risk score. The presence of MAL (rs8177374) allele T in the patient, absence of glucocorticoid receptor haplotype (consisting of rs6198, rs33389 and rs33388) ACT in the patient and absence of heat- shock protein 70-hom (+2437) (rs2227956) allele C in the patient were associated with decreased survival time. When compared to the EBMT risk score, the scores combining EBMT risk score with the genetic factors had an improved correlation with clinical outcome and better separation of risk groups. A bootstrapping technique, involving repeated testing of a model using multiple validation sets, also revealed that the newly proposed model had improved predictive value when compared to the EBMT risk score alone. Results support the view that non-HLA poly-morphisms could be useful for pretransplant clinical assessment and provide evidence that polymorphisms in the recipient genotype may influence incoming donor cells, suppressing the initiation of the graft versus leukaemia effect and reducing survival."],["dc.identifier.doi","10.1111/iji.12295"],["dc.identifier.isi","000393312700007"],["dc.identifier.pmid","27870355"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38762"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1744-313X"],["dc.relation.issn","1744-3121"],["dc.title","Impact of genomic risk factors on survival after haematopoietic stem cell transplantation for patients with acute leukaemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1445"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","1452"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Balavarca, Yesilda"],["dc.contributor.author","Pearce, Kim F."],["dc.contributor.author","Norden, J."],["dc.contributor.author","Collin, M."],["dc.contributor.author","Jackson, Graham H."],["dc.contributor.author","Holler, Ernst"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Kolb, H-J"],["dc.contributor.author","Greinix, Hildegard T."],["dc.contributor.author","Socie, G."],["dc.contributor.author","Toubert, A."],["dc.contributor.author","Rocha, Vanderson"],["dc.contributor.author","Gluckman, E."],["dc.contributor.author","Hromadnikova, Ilona"],["dc.contributor.author","Sedlacek, Petr"],["dc.contributor.author","Wolff, Daniel"],["dc.contributor.author","Holtick, U."],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Bickeboeller, Heike"],["dc.date.accessioned","2018-11-07T09:49:13Z"],["dc.date.available","2018-11-07T09:49:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Previous studies of non-histocompatibility leukocyte antigen (HLA) gene single-nucleotide polymorphisms (SNPs) on subgroups of patients undergoing allogeneic haematopoietic stem cell transplantation (HSCT) revealed an association with transplant outcome. This study further evaluated the association of non-HLA polymorphisms with overall survival in a cohort of 762 HSCT patients using data on 26 polymorphisms in 16 non-HLA genes. When viewed in addition to an already established clinical risk score (EBMT-score), three polymorphisms: rs8177374 in the gene for MyD88-adapter-like (MAL; P = 0.026), rs9340799 in the oestrogen receptor gene (ESR; P = 0.003) and rs1800795 in interleukin-6 (IL-6; P = 0.007) were found to be associated with reduced overall survival, whereas the haplo-genotype (ACC/ACC) in IL-10 was protective (P = 0.02). The addition of these non-HLA polymorphisms in a Cox regression model alongside the EBMT-score improved discrimination between risk groups and increased the level of prediction compared with the EBMT-score alone (gain in prediction capability for EBMT-genetic-score 10.8%). Results also demonstrated how changes in clinical practice through time have altered the effects of non-HLA analysis. The study illustrates the significance of non-HLA genotyping prior to HSCT and the importance of further investigation into non-HLA gene polymorphisms in risk prediction."],["dc.identifier.doi","10.1038/bmt.2015.173"],["dc.identifier.isi","000368281800008"],["dc.identifier.pmid","26214138"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35461"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1476-5365"],["dc.relation.issn","0268-3369"],["dc.title","Predicting survival using clinical risk scores and non-HLA immunogenetics"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","361"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Jalapothu, Dasaradha"],["dc.contributor.author","Boieri, Margherita"],["dc.contributor.author","Crossland, Rachel E."],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Butt, Isha A."],["dc.contributor.author","Norden, Jean"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Inngjerdingen, Marit"],["dc.date.accessioned","2018-11-07T10:08:30Z"],["dc.date.available","2018-11-07T10:08:30Z"],["dc.date.issued","2016"],["dc.description.abstract","MicroRNAs (miRNA) have emerged as central regulators of diverse biological processes and contribute to driving pathology in several diseases. Acute graft-versus-host disease (aGvHD) represents a major complication after allogeneic hematopoietic stem cell transplantation, caused by alloreactive donor T cells attacking host tissues leading to inflammation and tissue destruction. Changes in miRNA expression patterns occur during aGvHD, and we hypothesized that we could identify miRNA signatures in target tissues of aGvHD that may potentially help understand the underlying molecular pathology of the disease. We utilized a rat model of aGvHD with transplantation of fully MHC-mismatched T cell depleted bone marrow, followed by infusion of donor T cells. The expression pattern of 423 rat miRNAs was investigated in skin, gut, and lung tissues and intestinal T cells with the NanoString hybridization platform, in combination with validation by quantitative PCR. MHC-matched transplanted rats were included as controls. In the skin, upregulation of miR-34b and downregulation of miR-326 was observed, while in the intestines, we detected downregulation of miR-743b and a trend toward downregulation of miR-345-5p. Thus, tissue-specific expression patterns of miRNAs were observed. Neither miR-326 nor miR-743b has previously been associated with aGvHD. Moreover, we identified upregulation of miR-146a and miR-155 in skin tissue of rats suffering from aGvHD. Analysis of intestinal T cells indicated 23 miRNAs differentially regulated between aGvHD and controls. Two of these miRNAs were differentially expressed either in skin (miR-326) or in intestinal (miR-345-5p) tissue. Comparison of intestinal and peripheral blood T cells indicated common dysregulated expression of miR-99a, miR-223, miR-326, and miR-345-5p. Analysis of predicted gene targets for these miRNAs indicated potential targeting of an inflammatory network both in skin and in the intestines that may further regulate inflammatory cytokine production. In conclusion, comprehensive miRNA profiling in rats suffering from aGvHD demonstrate tissue-specific differences in the expression patterns of miRNA that may not be detected by profiling of peripheral blood T cells alone. These tissue-specific miRNAs may contribute to distinct pathologic mechanisms and could represent potential targets for therapy."],["dc.description.sponsorship","European Union [FP7-PEOPLE-2012-ITN-315963]"],["dc.identifier.doi","10.3389/fimmu.2016.00361"],["dc.identifier.isi","000383320200001"],["dc.identifier.pmid","27695455"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13746"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39474"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Media Sa"],["dc.relation.issn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Tissue-specific expression Patterns of Microrna during acute graft-versus-host Disease in the rat"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e16582"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Novota, Peter"],["dc.contributor.author","Zinocker, Severin"],["dc.contributor.author","Norden, Jean"],["dc.contributor.author","Wang, X."],["dc.contributor.author","Sviland, Lisbet"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Rolstad, Bent"],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:00:02Z"],["dc.date.available","2018-11-07T09:00:02Z"],["dc.date.issued","2011"],["dc.description.abstract","Background: The major histocompatibility complex (MHC) is the most important genomic region that contributes to the risk of graft versus host disease (GVHD) after haematopoietic stem cell transplantation. Matching of MHC class I and II genes is essential for the success of transplantation. However, the MHC contains additional genes that also contribute to the risk of developing acute GVHD. It is difficult to identify these genes by genetic association studies alone due to linkage disequilibrium in this region. Therefore, we aimed to identify MHC genes and other genes involved in the pathophysiology of GVHD by mRNA expression profiling. Methodology/Principal Findings: To reduce the complexity of the task, we used genetically well-defined rat inbred strains and a rat skin explant assay, an in-vitro-model of the graft versus host reaction (GVHR), to analyze the expression of MHC, natural killer complex (NKC), and other genes in cutaneous GVHR. We observed a statistically significant and strong up or down regulation of 11 MHC, 6 NKC, and 168 genes encoded in other genomic regions, i.e. 4.9%, 14.0%, and 2.6% of the tested genes respectively. The regulation of 7 selected MHC and 3 NKC genes was confirmed by quantitative real-time PCR and in independent skin explant assays. In addition, similar regulations of most of the selected genes were observed in GVHD-affected skin lesions of transplanted rats and in human skin explant assays. Conclusions/Significance: We identified rat and human MHC and NKC genes that are regulated during GVHR in skin explant assays and could therefore serve as biomarkers for GVHD. Several of the respective human genes, including HLA-DMB, C2, AIF1, SPR1, UBD, and OLR1, are polymorphic. These candidates may therefore contribute to the genetic risk of GVHD in patients."],["dc.identifier.doi","10.1371/journal.pone.0016582"],["dc.identifier.isi","000286664100046"],["dc.identifier.pmid","21305040"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24049"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Expression Profiling of Major Histocompatibility and Natural Killer Complex Genes Reveals Candidates for Controlling Risk of Graft versus Host Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Tissue Antigens"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Novota, P."],["dc.contributor.author","Zinocker, Severin"],["dc.contributor.author","Norden, J."],["dc.contributor.author","Wang, X. N."],["dc.contributor.author","Sviland, Lisbet"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Rolstad, Bent"],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Walter, L."],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T08:56:48Z"],["dc.date.available","2018-11-07T08:56:48Z"],["dc.date.issued","2011"],["dc.format.extent","381"],["dc.identifier.isi","000289249000030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23237"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.conference","25th Conference on European Immunogenetics and Histocompatibility"],["dc.relation.eventlocation","Prague, CZECH REPUBLIC"],["dc.relation.issn","0001-2815"],["dc.title","Expression profiling of major histocompatibility and natural killer complex genes reveals new candidates for controlling risk of graft versus host disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]