Odoardi, Francesca

[["dc.bibliographiccitation.firstpage","117"],["dc.bibliographiccitation.lastpage","129"],["dc.contributor.author","Schläger, Christian"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.editor","Weissert, Robert"],["dc.date.accessioned","2020-07-06T13:57:37Z"],["dc.date.available","2020-07-06T13:57:37Z"],["dc.date.issued","2016"],["dc.description.abstract","The CNS is effectively shielded from the periphery by the blood-brain barrier (BBB) which limits the entry of cells and solutes. However, in autoimmune disorders such as multiple sclerosis, immune cells can overcome this barrier and induce the formation of CNS inflammatory lesions. Recently, two-photon laser scanning microscopy (TPLSM) has made it possible to visualize autoimmune processes in the living CNS in real time. However, along with a high microscopy standard, this technique requires an advanced surgical procedure to access the region of interest. Here, we describe in detail the necessary methodological steps to visualize (auto)immune processes in living rodent tissue. We focus on the procedures to image the leptomeningeal vessels of the thoracic spinal cord during transfer experimental autoimmune encephalomyelitis in LEW rats (AT EAE) and in active EAE in C57BL/6 mice (aEAE)."],["dc.identifier.doi","10.1007/7651_2014_150"],["dc.identifier.pmid","25549830"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66861"],["dc.language.iso","en"],["dc.publisher","Springer"],["dc.relation.ispartof","Multiple Sclerosis: Methods and Protocols"],["dc.title","In Vivo Visualization of (Auto)Immune Processes in the Central Nervous System of Rodents"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1805"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Experimental Medicine"],["dc.bibliographiccitation.lastpage","1814"],["dc.bibliographiccitation.volume","201"],["dc.contributor.author","Kawakami, Naoto"],["dc.contributor.author","Nägerl, U Valentin"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Bonhoeffer, Tobias"],["dc.contributor.author","Wekerle, Hartmut"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-07-06T13:58:17Z"],["dc.date.available","2020-07-06T13:58:17Z"],["dc.date.issued","2005-06-06"],["dc.description.abstract","We tracked pathogenic myelin basic protein-specific CD4+ effector T cells in early central nervous system (CNS) lesions of experimental autoimmune encephalomyelitis (EAE) by combining two-photon imaging and fluorescence video microscopy. We made two key observations: (a) the majority of the cells (65%) moved fast (maximal speed 25 microm/min) and apparently nondirected through the compact tissue; and (b) a second group of effector T cells (35%) appeared tethered to a fixed point. Polarization of T cell receptor and adhesion molecules (lymphocyte function-associated antigen 1) towards this fixed point suggests the formation of immune synapses. Nonpathogenic, ovalbumin-specific T cells were not tethered in the CNS and did not form synapse-like contacts, but moved through the tissue. After intrathecal injection of antigen, 40% of ovalbumin-specific T cells became tethered. Conversely, injection of anti-major histocompatibility complex class II antibodies profoundly reduced the number of stationary pathogenic T cells within the CNS (to 15%). We propose that rapid penetration of the CNS parenchyma by numerous autoimmune effector T cells along with multiple autoantigen-presentation events are responsible for the fulminate development of clinical EAE."],["dc.identifier.doi","10.1084/jem.20050011"],["dc.identifier.pmid","15939794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66867"],["dc.language.iso","en"],["dc.relation.issn","0022-1007"],["dc.title","Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","105"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","118"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Puchert, Malte"],["dc.contributor.author","Pelkner, Fabian"],["dc.contributor.author","Stein, Gregor"],["dc.contributor.author","Angelov, Doychin N"],["dc.contributor.author","Boltze, Johannes"],["dc.contributor.author","Wagner, Daniel-Christoph"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Streit, Wolfgang J"],["dc.contributor.author","Engele, Jürgen"],["dc.date.accessioned","2020-07-06T13:57:26Z"],["dc.date.available","2020-07-06T13:57:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Based on our previous demonstration of CXCR7 as the major mediator of CXCL12 signaling in cultured astrocytes, we have now compared astrocytic expression of the CXCL12 receptors, CXCR7 and CXCR4, during CNS development and disease. In addition, we asked whether disease-associated conditions/factors affect expression of CXCL12 receptors in astrocytes. In the late embryonic rat brain, CXCR7+/GFAP+ cells were restricted to the ventricular/subventricular zone while CXCR4 was widely absent from GFAP-positive cells. In the early postnatal and adult brain, CXCR7 and CXCR4 were almost exclusively expressed by GFAP-immunoreactive astrocytes forming the superficial glia limitans. Contrasting the situation in the intact CNS, a striking increase in astrocytic CXCR7 expression was detectable in the cortex of rats with experimental brain infarcts, in the spinal cord of rats with experimental autoimmune encephalomyelitis (EAE) and after mechanical compression, as well as in the in infarcted human cerebral cortex and in the hippocampus of Alzheimer's disease patients. None of these pathologies was associated with substantial increases in astrocytic CXCR4 expression. Screening of various disease-associated factors/conditions further revealed that CXCR7 expression of cultured cortical astrocytes increases with IFNγ as well as under hypoxic conditions whereas CXCR7 expression is attenuated following treatment with IFNβ. Again, none of the treatments affected CXCR4 expression in cultured astrocytes. Together, these findings support the hypothesis of a crucial role of astrocytic CXCR7 in the progression of various CNS pathologies."],["dc.identifier.doi","10.1016/j.mcn.2017.09.001"],["dc.identifier.pmid","28889992"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66859"],["dc.language.iso","en"],["dc.relation.eissn","1095-9327"],["dc.relation.issn","1044-7431"],["dc.title","Astrocytic expression of the CXCL12 receptor, CXCR7/ACKR3 is a hallmark of the diseased, but not developing CNS"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","69"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","81"],["dc.bibliographiccitation.volume","175"],["dc.contributor.author","Kawakami, Naoto"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Bradl, Monika"],["dc.contributor.author","Ritter, Thomas"],["dc.contributor.author","Neuhaus, Oliver"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Wekerle, Hartmut"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-07-06T13:58:28Z"],["dc.date.available","2020-07-06T13:58:28Z"],["dc.date.issued","2005-07-01"],["dc.description.abstract","We embedded green fluorescent CD4(+) T cells specific for myelin basic protein (MBP) (T(MBP-GFP) cells) in the immune system of syngeneic neonatal rats. These cells persisted in the animals for the entire observation period spanning >2 years without affecting the health of the hosts. They maintained a memory phenotype with low levels of L-selectin and CD45RC, but high CD44. Although persisting in low numbers (0.01-0.1% of lymph node cells) they were sufficient to raise susceptibility toward clinical autoimmune disease. Immunization with MBP in IFA induced CNS inflammation and overt clinical disease in animals carrying neonatally transferred T(MBP-GFP) cells, but not in controls. The onset of the clinical disease coincided with mass infiltration of T(MBP-GFP) cells into the CNS. In the periphery, following the amplification phase a rapid contraction of the T cell population was observed. However, elevated numbers of fully reactive T(MBP-GFP) cells remained in the peripheral immune system after acute experimental autoimmune encephalomyelitis mediating reimmunization-induced disease relapses."],["dc.identifier.doi","10.4049/jimmunol.175.1.69"],["dc.identifier.pmid","15972633"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66869"],["dc.language.iso","en"],["dc.relation.issn","0022-1767"],["dc.title","Autoimmune CD4+ T cell memory: lifelong persistence of encephalitogenic T cell clones in healthy immune repertoires"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","138"],["dc.bibliographiccitation.issue","7899"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","144"],["dc.bibliographiccitation.volume","603"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Canals, Roger Cugota"],["dc.contributor.author","van der Flier, Felicia Joy"],["dc.contributor.author","Hollensteiner, Jacqueline"],["dc.contributor.author","Daniel, Rolf"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Odoardi, Francesca"],["dc.date.accessioned","2022-04-01T10:00:47Z"],["dc.date.available","2022-04-01T10:00:47Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1038/s41586-022-04427-4"],["dc.identifier.pii","4427"],["dc.identifier.pmid","35197636"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105512"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/58"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["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.eissn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.relation.workinggroup","RG Flügel"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","The lung microbiome regulates brain autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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.firstpage","1021"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cell Research"],["dc.bibliographiccitation.lastpage","1022"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Neuhuber, Winfried"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-07-06T13:57:47Z"],["dc.date.available","2020-07-06T13:57:47Z"],["dc.date.issued","2014-09"],["dc.description.abstract","A recent paper published in Nature reports sensory nerve fibers in the skin that give local immune cells important instructions for the organization of an immune response; in this particular case the cooperation between the nervous and immune systems had disastrous consequences, namely an auto-destruction of the skin."],["dc.identifier.doi","10.1038/cr.2014.80"],["dc.identifier.pmid","24946740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66862"],["dc.language.iso","en"],["dc.relation.eissn","1748-7838"],["dc.relation.issn","1001-0602"],["dc.title","Pain-induced skin autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","97"],["dc.bibliographiccitation.volume","191"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Nosov, Mikhail"],["dc.contributor.author","Kawakami, Naoto"],["dc.date.accessioned","2020-07-06T13:57:58Z"],["dc.date.available","2020-07-06T13:57:58Z"],["dc.date.issued","2007-11"],["dc.description.abstract","Two photon microscopy (TPM) recently emerged as optical tool for the visualization of immune processes hundreds of micrometers deep in living tissue and organs. Here we summarize recent work on exploiting this technology to study brain antigen specific T cells. These cells are the cause of Experimental Autoimmune Encephalomyelitis (EAE) an autoimmune disease model of Multiple Sclerosis. TPM studies elucidated the dynamics of the autoaggressive effector T cells in peripheral immune milieus during preclinical EAE, where the cells become reprogrammed to enter their target organ. These studies revealed an unexpectedly lively locomotion behavior of the cells interrupted only by short-lasting contacts with the local immune stroma. Live T cell behavior was furthermore studied within the acutely inflamed CNS. Two distinct migratory patterns of the T cells were found: the majority of cells (60-70%) moved fast and seemingly unhindered through the compact CNS parenchyma. The motility of the other cell fraction was highly confined. The cells swung around a fixed cell pole forming long-lasting contacts to putative local antigen presenting cells."],["dc.identifier.doi","10.1016/j.jneuroim.2007.09.017"],["dc.identifier.pmid","17976745"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66864"],["dc.language.iso","en"],["dc.relation.issn","0165-5728"],["dc.title","Autoaggressive effector T cells in the course of experimental autoimmune encephalomyelitis visualized in the light of two-photon microscopy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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","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"]]