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  1. AU="Janos Groh"
  2. AU="Prakash, Nishant"
  3. AU="Loew, Thomas"
  4. AU=Kroemer Guido
  5. AU="Bomonetto, Juliana Vieira Biason"
  6. AU="Benavides-González, Mario Alberto"
  7. AU="Matsuo, Kazuya"
  8. AU="Yaniv, Ziv"
  9. AU="Robertson, Anne"
  10. AU="Davis, Rebecca"
  11. AU="Joy, Tisha R"
  12. AU="Özil, Musa"
  13. AU="Franci, Lorenzo"
  14. AU="Khoobdel, Mehdi"
  15. AU="Ian B Wilkinson"
  16. AU="Sarpün, I.H."
  17. AU="Gums, Jeremiah J"
  18. AU="Petsalaki, Eleni"
  19. AU="Yu, Weichao"
  20. AU="Mertens, Anne Wiebke"
  21. AU="Roitershtein, Alexander"
  22. AU="Deppen, Stephen"
  23. AU="Goliath, Rene"
  24. AU="Emons, Günter"
  25. AU="Sarah S. Barnett"

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  1. Artikel ; Online: Cytotoxic CNS-associated T cells drive axon degeneration by targeting perturbed oligodendrocytes in PLP1 mutant mice

    Tassnim Abdelwahab / David Stadler / Konrad Knöpper / Panagiota Arampatzi / Antoine-Emmanuel Saliba / Wolfgang Kastenmüller / Rudolf Martini / Janos Groh

    iScience, Vol 26, Iss 5, Pp 106698- (2023)

    2023  

    Abstract: Summary: Myelin defects lead to neurological dysfunction in various diseases and in normal aging. Chronic neuroinflammation often contributes to axon-myelin damage in these conditions and can be initiated and/or sustained by perturbed myelinating glia. ... ...

    Abstract Summary: Myelin defects lead to neurological dysfunction in various diseases and in normal aging. Chronic neuroinflammation often contributes to axon-myelin damage in these conditions and can be initiated and/or sustained by perturbed myelinating glia. We have previously shown that distinct PLP1 mutations result in neurodegeneration that is largely driven by adaptive immune cells. Here we characterize CD8+ CNS-associated T cells in myelin mutants using single-cell transcriptomics and identify population heterogeneity and disease-associated changes. We demonstrate that early sphingosine-1-phosphate receptor modulation attenuates T cell recruitment and neural damage, while later targeting of CNS-associated T cell populations is inefficient. Applying bone marrow chimerism and utilizing random X chromosome inactivation, we provide evidence that axonal damage is driven by cytotoxic, antigen specific CD8+ T cells that target mutant myelinating oligodendrocytes. These findings offer insights into neural-immune interactions and are of translational relevance for neurological conditions associated with myelin defects and neuroinflammation.
    Schlagwörter Molecular neuroscience ; Components of the immune system ; Model organism ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2023-05-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Microglia-mediated demyelination protects against CD8+ T cell-driven axon degeneration in mice carrying PLP defects

    Janos Groh / Tassnim Abdelwahab / Yogita Kattimani / Michaela Hörner / Silke Loserth / Viktoria Gudi / Robert Adalbert / Fabian Imdahl / Antoine-Emmanuel Saliba / Michael Coleman / Martin Stangel / Mikael Simons / Rudolf Martini

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Band 21

    Abstract: Abstract Axon degeneration and functional decline in myelin diseases are often attributed to loss of myelin but their relation is not fully understood. Perturbed myelinating glia can instigate chronic neuroinflammation and contribute to demyelination and ...

    Abstract Abstract Axon degeneration and functional decline in myelin diseases are often attributed to loss of myelin but their relation is not fully understood. Perturbed myelinating glia can instigate chronic neuroinflammation and contribute to demyelination and axonal damage. Here we study mice with distinct defects in the proteolipid protein 1 gene that develop axonal damage which is driven by cytotoxic T cells targeting myelinating oligodendrocytes. We show that persistent ensheathment with perturbed myelin poses a risk for axon degeneration, neuron loss, and behavioral decline. We demonstrate that CD8+ T cell-driven axonal damage is less likely to progress towards degeneration when axons are efficiently demyelinated by activated microglia. Mechanistically, we show that cytotoxic T cell effector molecules induce cytoskeletal alterations within myelinating glia and aberrant actomyosin constriction of axons at paranodal domains. Our study identifies detrimental axon-glia-immune interactions which promote neurodegeneration and possible therapeutic targets for disorders associated with myelin defects and neuroinflammation.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2023-10-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Brain-to-gut trafficking of alpha-synuclein by CD11c+ cells in a mouse model of Parkinson’s disease

    Rhonda L. McFleder / Anastasiia Makhotkina / Janos Groh / Ursula Keber / Fabian Imdahl / Josefina Peña Mosca / Alina Peteranderl / Jingjing Wu / Sawako Tabuchi / Jan Hoffmann / Ann-Kathrin Karl / Axel Pagenstecher / Jörg Vogel / Andreas Beilhack / James B. Koprich / Jonathan M. Brotchie / Antoine-Emmanuel Saliba / Jens Volkmann / Chi Wang Ip

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Band 13

    Abstract: Abstract Inflammation in the brain and gut is a critical component of several neurological diseases, such as Parkinson’s disease (PD). One trigger of the immune system in PD is aggregation of the pre-synaptic protein, α-synuclein (αSyn). Understanding ... ...

    Abstract Abstract Inflammation in the brain and gut is a critical component of several neurological diseases, such as Parkinson’s disease (PD). One trigger of the immune system in PD is aggregation of the pre-synaptic protein, α-synuclein (αSyn). Understanding the mechanism of propagation of αSyn aggregates is essential to developing disease-modifying therapeutics. Using a brain-first mouse model of PD, we demonstrate αSyn trafficking from the brain to the ileum of male mice. Immunohistochemistry revealed that the ileal αSyn aggregations are contained within CD11c+ cells. Using single-cell RNA sequencing, we demonstrate that ileal CD11c+ cells are microglia-like and the same subtype of cells is activated in the brain and ileum of PD mice. Moreover, by utilizing mice expressing the photo-convertible protein, Dendra2, we show that CD11c+ cells traffic from the brain to the ileum. Together these data provide a mechanism of αSyn trafficking between the brain and gut.
    Schlagwörter Science ; Q
    Thema/Rubrik (Code) 612
    Sprache Englisch
    Erscheinungsdatum 2023-11-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Secretome Analysis of Mesenchymal Stem Cell Factors Fostering Oligodendroglial Differentiation of Neural Stem Cells In Vivo

    Iria Samper Agrelo / Jessica Schira-Heinen / Felix Beyer / Janos Groh / Christine Bütermann / Veronica Estrada / Gereon Poschmann / Ana Bribian / Janusz J. Jadasz / Laura Lopez-Mascaraque / David Kremer / Rudolf Martini / Hans Werner Müller / Hans Peter Hartung / James Adjaye / Kai Stühler / Patrick Küry

    International Journal of Molecular Sciences, Vol 21, Iss 4350, p

    2020  Band 4350

    Abstract: Mesenchymal stem cell (MSC)-secreted factors have been shown to significantly promote oligodendrogenesis from cultured primary adult neural stem cells (aNSCs) and oligodendroglial precursor cells (OPCs). Revealing underlying mechanisms of how aNSCs can ... ...

    Abstract Mesenchymal stem cell (MSC)-secreted factors have been shown to significantly promote oligodendrogenesis from cultured primary adult neural stem cells (aNSCs) and oligodendroglial precursor cells (OPCs). Revealing underlying mechanisms of how aNSCs can be fostered to differentiate into a specific cell lineage could provide important insights for the establishment of novel neuroregenerative treatment approaches aiming at myelin repair. However, the nature of MSC-derived differentiation and maturation factors acting on the oligodendroglial lineage has not been identified thus far. In addition to missing information on active ingredients, the degree to which MSC-dependent lineage instruction is functional in vivo also remains to be established. We here demonstrate that MSC-derived factors can indeed stimulate oligodendrogenesis and myelin sheath generation of aNSCs transplanted into different rodent central nervous system (CNS) regions, and furthermore, we provide insights into the underlying mechanism on the basis of a comparative mass spectrometry secretome analysis. We identified a number of secreted proteins known to act on oligodendroglia lineage differentiation. Among them, the tissue inhibitor of metalloproteinase type 1 (TIMP-1) was revealed to be an active component of the MSC-conditioned medium, thus validating our chosen secretome approach.
    Schlagwörter neural stem cells ; mesenchymal stem cells ; transplantation ; oligodendroglia ; glial fate modulation ; myelin ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2020-06-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.

    Chi Wang Ip / Antje Kroner / Janos Groh / Marianne Huber / Dennis Klein / Irene Spahn / Ricarda Diem / Sarah K Williams / Klaus-Armin Nave / Julia M Edgar / Rudolf Martini

    PLoS ONE, Vol 7, Iss 8, p e

    2012  Band 42554

    Abstract: Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected ... ...

    Abstract Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow transfer from wildtype mice, but not from perforin- or granzyme B-deficient mutants, into lymphocyte-deficient PLP mutant mice led again to impaired axonal transport and the formation of axonal swellings, which are predominantly located at the juxtaparanodal region. This demonstrates that the adaptive immune system, including cytotoxic T-lymphocytes which release perforin and granzyme B, are necessary to perturb axonal integrity in the PLP-transgenic disease model. Based on our observations, so far not attended molecular and cellular players belonging to the immune system should be considered to understand pathogenesis in inherited myelin disorders with progressive axonal damage.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 006
    Sprache Englisch
    Erscheinungsdatum 2012-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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