Odoardi, Francesca

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Gao, Ming"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Thal, Dietmar R."],["dc.contributor.author","Chang, Mayland"],["dc.contributor.author","Opdenakker, Ghislain"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:28:11Z"],["dc.date.available","2021-04-14T08:28:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1172/JCI141694"],["dc.identifier.pmid","33645550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82526"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/22"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

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

[["dc.bibliographiccitation.firstpage","349"],["dc.bibliographiccitation.issue","7590"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","530"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Vidoli, Stefano"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Mielke, Dorothee"],["dc.contributor.author","Brylla, Elke"],["dc.contributor.author","Issekutz, Thomas B."],["dc.contributor.author","Cabanas, Carlos"],["dc.contributor.author","Nelsons, Peter J."],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T10:18:08Z"],["dc.date.available","2018-11-07T10:18:08Z"],["dc.date.issued","2016"],["dc.description.abstract","In multiple sclerosis, brain-reactive T cells invade the central nervous system (CNS) and induce a self-destructive inflammatory process. T-cell infiltrates are not only found within the parenchyma and the meninges, but also in the cerebrospinal fluid (CSF) that bathes the entire CNS tissue(1,2). How the T cells reach the CSF, their functionality, and whether they traffic between the CSF and other CNS compartments remains hypothetical(3-6). Here we show that effector T cells enter the CSF from the leptomeninges during Lewis rat experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. While moving through the three-dimensional leptomeningeal network of collagen fibres in a random Brownian walk, T cells were flushed from the surface by the flow of the CSF. The detached cells displayed significantly lower activation levels compared to T cells from the leptomeninges and CNS parenchyma. However, they did not represent a specialized non-pathogenic cellular sub-fraction, as their gene expression profile strongly resembled that of tissue-derived T cells and they fully retained their encephalitogenic potential. T-cell detachment from the leptomeninges was counteracted by integrins VLA-4 and LFA-1 binding to their respective ligands produced by resident macrophages. Chemokine signalling via CCR5/CXCR3 and antigenic stimulation of T cells in contact with the leptomeningeal macrophages enforced their adhesiveness. T cells floating in the CSF were able to reattach to the leptomeninges through steps reminiscent of vascular adhesion in CNS blood vessels, and invade the parenchyma. The molecular/cellular conditions for T-cell reattachment were the same as the requirements for detachment from the leptomeningeal milieu. Our data indicate that the leptomeninges represent a checkpoint at which activated T cells are licensed to enter the CNS parenchyma and non-activated T cells are preferentially released into the CSF, from where they can reach areas of antigen availability and tissue damage."],["dc.identifier.doi","10.1038/nature16939"],["dc.identifier.isi","000370327100040"],["dc.identifier.pmid","26863192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41367"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.title","Effector T-cell trafficking between the leptomeninges and the cerebrospinal fluid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E15"],["dc.bibliographiccitation.issue","7749"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","E15"],["dc.bibliographiccitation.volume","567"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Hermann, Moritz"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Flügel-Koch, Cassandra"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Schlosser, Corinna"],["dc.contributor.author","Merlini, Arianna"],["dc.contributor.author","Körner, Henrike"],["dc.contributor.author","Chang, Hsin-Fang"],["dc.contributor.author","Fischer, Henrike J"],["dc.contributor.author","Reichardt, Holger M"],["dc.contributor.author","Zagrebelsky, Marta"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-07-06T13:57:21Z"],["dc.date.available","2020-07-06T13:57:21Z"],["dc.date.issued","2019-03"],["dc.description.abstract","In this Article, owing to an error during the production process, the y-axis label of Fig. 2c should read \"Number of Tβ-syn cells\" rather than \"Number of T1β-syn cells\" and the left and right panels of Fig. 4 should be labelled 'a' and 'b', respectively. These errors have been corrected online."],["dc.identifier.doi","10.1038/s41586-019-1047-0"],["dc.identifier.pmid","30867589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66858"],["dc.language.iso","en"],["dc.relation.eissn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.title","Publisher Correction: β-Synuclein-reactive T cells induce autoimmune CNS grey matter degeneration"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:33:36Z"],["dc.date.available","2018-11-07T09:33:36Z"],["dc.date.issued","2014"],["dc.format.extent","204"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.548"],["dc.identifier.isi","000345192100537"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32001"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","In vivo visualization of the role of chemokines in migratory T cells during CNS inflammation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","503"],["dc.bibliographiccitation.issue","7745"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","508"],["dc.bibliographiccitation.volume","566"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Hermann, Moritz"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Flügel-Koch, Cassandra"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Schlosser, Corinna"],["dc.contributor.author","Merlini, Arianna"],["dc.contributor.author","Körner, Henrike"],["dc.contributor.author","Chang, Hsin-Fang"],["dc.contributor.author","Fischer, Henrike J"],["dc.contributor.author","Reichardt, Holger M"],["dc.contributor.author","Zagrebelsky, Marta"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-06-29T07:08:43Z"],["dc.date.available","2020-06-29T07:08:43Z"],["dc.date.issued","2019"],["dc.description.abstract","The grey matter is a central target of pathological processes in neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. The grey matter is often also affected in multiple sclerosis, an autoimmune disease of the central nervous system. The mechanisms that underlie grey matter inflammation and degeneration in multiple sclerosis are not well understood. Here we show that, in Lewis rats, T cells directed against the neuronal protein β-synuclein specifically invade the grey matter and that this is accompanied by the presentation of multifaceted clinical disease. The expression pattern of β-synuclein induces the local activation of these T cells and, therefore, determined inflammatory priming of the tissue and targeted recruitment of immune cells. The resulting inflammation led to significant changes in the grey matter, which ranged from gliosis and neuronal destruction to brain atrophy. In humans, β-synuclein-specific T cells were enriched in patients with chronic-progressive multiple sclerosis. These findings reveal a previously unrecognized role of β-synuclein in provoking T-cell-mediated pathology of the central nervous system."],["dc.identifier.doi","10.1038/s41586-019-0964-2"],["dc.identifier.pmid","30787438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66760"],["dc.language.iso","en"],["dc.relation.eissn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.title","β-Synuclein-reactive T cells induce autoimmune CNS grey matter degeneration"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3323"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","3328"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Gomez, Cesar Cordero"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Fehling, Hans-Joerg"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T10:16:44Z"],["dc.date.available","2018-11-07T10:16:44Z"],["dc.date.issued","2016"],["dc.description.abstract","Multiple sclerosis (MS) is caused by T cells that are reactive for brain antigens. In experimental autoimmune encephalomyelitis, the animal model for MS, myelin-reactive T cells initiate the autoimmune process when entering the nervous tissue and become reactivated upon local encounter of their cognate CNS antigen. Thereby, the strength of the T-cellular reactivation process within the CNS tissue is crucial for the manifestation and the severity of the clinical disease. Recently, B cells were found to participate in the pathogenesis of CNS autoimmunity, with several diverse underlying mechanisms being under discussion. We here report that B cells play an important role in promoting the initiation process of CNS autoimmunity. Myelin-specific antibodies produced by autoreactive B cells after activation in the periphery diffused into the CNS together with the first invading pathogenic T cells. The antibodies accumulated in resident antigen-presenting phagocytes and significantly enhanced the activation of the incoming effector T cells. The ensuing strong blood-brain barrier disruption and immune cell recruitment resulted in rapid manifestation of clinical disease. Therefore, myelin oligodendrocyte glycoprotein (MOG)-specific autoantibodies can initiate disease bouts by cooperating with the autoreactive T cells in helping them to recognize their autoantigen and become efficiently reactivated within the immune-deprived nervous tissue."],["dc.identifier.doi","10.1073/pnas.1519608113"],["dc.identifier.isi","000372488200061"],["dc.identifier.pmid","26957602"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41093"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Autoantibody-boosted T-cell reactivation in the target organ triggers manifestation of autoimmune CNS disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","887"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","899"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Merlini, Arianna"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Strauß, Judith"],["dc.contributor.author","Hildebrand, Luisa"],["dc.contributor.author","Genc, Nafiye"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Chilov, Dmitri"],["dc.contributor.author","Alitalo, Kari"],["dc.contributor.author","Flügel-Koch, Cassandra"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Odoardi, Francesca"],["dc.date.accessioned","2022-08-19T08:14:13Z"],["dc.date.available","2022-08-19T08:14:13Z"],["dc.date.issued","2022-07"],["dc.description.abstract","The meninges, comprising the leptomeninges (pia and arachnoid layers) and the pachymeninx (dura layer), participate in central nervous system (CNS) autoimmunity, but their relative contributions remain unclear. Here we report on findings in animal models of CNS autoimmunity and in patients with multiple sclerosis, where, in acute and chronic disease, the leptomeninges were highly inflamed and showed structural changes, while the dura mater was only marginally affected. Although dural vessels were leakier than leptomeningeal vessels, effector T cells adhered more weakly to the dural endothelium. Furthermore, local antigen-presenting cells presented myelin and neuronal autoantigens less efficiently, and the activation of autoreactive T cells was lower in dural than leptomeningeal layers, preventing local inflammatory processes. Direct antigen application was required to evoke a local inflammatory response in the dura. Together, our data demonstrate an uneven involvement of the meningeal layers in CNS autoimmunity, in which effector T cell trafficking and activation are functionally confined to the leptomeninges, while the dura remains largely excluded from CNS autoimmune processes."],["dc.identifier.doi","10.1038/s41593-022-01108-3"],["dc.identifier.pmid","35773544"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113030"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/71"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/510"],["dc.language.iso","en"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A03: Checkpoints determining recovery from acute autoimmune CNS grey matter lesions"],["dc.relation","TRR 274 | A04: The role of the meninges in the resolution of acute autoimmune CNS lesions"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1546-1726"],["dc.relation.issn","1097-6256"],["dc.relation.workinggroup","RG Flügel"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Distinct roles of the meningeal layers in CNS autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","784"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","Kitz, Alexandra"],["dc.contributor.author","Nosov, Michail"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:24:11Z"],["dc.date.available","2018-11-07T09:24:11Z"],["dc.date.issued","2013"],["dc.description.abstract","Multiple sclerosis is an autoimmune disease of the central nervous system (CNS) that is initiated when self-reactive T cells enter the brain and become locally activated after encountering their specific nervous antigens. When and where the disease-relevant antigen encounters occur is unclear. Here we combined fluorescently labeled nuclear factor of activated T cells (NFAT) with histone protein H2B to create a broadly applicable molecular sensor for intravital imaging of T cell activation. In experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis, we report that effector T cells entering the CNS become activated after short contacts with leptomeningeal phagocytes. During established disease, the activation process is extended to the depth of the CNS parenchyma, where the cells form contacts with microglia and recruited phagocytes. We show that it is the activation processes during the preclinical phase rather than during established disease that are essential for the intensity and duration of the disease bout."],["dc.identifier.doi","10.1038/nm.3182"],["dc.identifier.isi","000319981600030"],["dc.identifier.pmid","23624600"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29760"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","A combination of fluorescent NFAT and H2B sensors uncovers dynamics of T cell activation in real time during CNS autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]