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  1. Book ; Thesis: Analysis of the anti-tumor immune response against sporadic cancers in LoxP-Tag transgenic mice

    Czéh, Melinda

    2008  

    Author's details by Melinda Czéh
    Language English
    Size 93 Bl., Ill., graph. Darst., 30 cm
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Berlin, Freie Univ., Diss., 2008
    HBZ-ID HT015761014
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2008 E 1751 order for loan Magazin

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  2. Article: Uncovering a new cellular origin for acute myeloid leukemia with lineage plasticity.

    Czeh, Melinda / Rosenbauer, Frank

    Molecular & cellular oncology

    2016  Volume 4, Issue 2, Page(s) e1268241

    Abstract: Although acute myeloid leukaemia (AML) is assumed to be driven by transformed haematopoietic stem and progenitor cells, we have described recently a new pathway leading to AML from T-cell progenitors. Furthermore, we could identify a subgroup of human ... ...

    Abstract Although acute myeloid leukaemia (AML) is assumed to be driven by transformed haematopoietic stem and progenitor cells, we have described recently a new pathway leading to AML from T-cell progenitors. Furthermore, we could identify a subgroup of human AML with gene expression profile suggesting T-lymphoid origin and potentially novel treatment.
    Language English
    Publishing date 2016-12-14
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2016.1268241
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: DNMT1 Deficiency Impacts on Plasmacytoid Dendritic Cells in Homeostasis and Autoimmune Disease.

    Czeh, Melinda / Stäble, Sina / Krämer, Stephen / Tepe, Lena / Talyan, Sweta / Carrelha, Joana / Meng, Yiran / Heitplatz, Barbara / Schwabenland, Marius / Milsom, Michael D / Plass, Christoph / Prinz, Marco / Schlesner, Matthias / Andrade-Navarro, Miguel A / Nerlov, Claus / Jacobsen, Sten Eirik W / Lipka, Daniel B / Rosenbauer, Frank

    Journal of immunology (Baltimore, Md. : 1950)

    2021  Volume 208, Issue 2, Page(s) 358–370

    Abstract: Dendritic cells (DCs) are heterogeneous immune regulators involved in autoimmune diseases. Epigenomic mechanisms orchestrating DC development and DC subset diversification remain insufficiently understood but could be important to modulate DC fate for ... ...

    Abstract Dendritic cells (DCs) are heterogeneous immune regulators involved in autoimmune diseases. Epigenomic mechanisms orchestrating DC development and DC subset diversification remain insufficiently understood but could be important to modulate DC fate for clinical purposes. By combining whole-genome methylation assessment with the analysis of mice expressing reduced DNA methyltransferase 1 levels, we show that distinct DNA methylation levels and patterns are required for the development of plasmacytoid DC and conventional DC subsets. We provide clonal in vivo evidence for DC lineage establishment at the stem cell level, and we show that a high DNA methylation threshold level is essential for Flt3-dependent survival of DC precursors. Importantly, reducing methylation predominantly depletes plasmacytoid DC and alleviates systemic lupus erythematosus in an autoimmunity mouse model. This study shows how DNA methylation regulates the production of DC subsets and provides a potential rationale for targeting autoimmune disease using hypomethylating agents.
    MeSH term(s) Animals ; Autoimmunity/genetics ; Bone Marrow Cells/immunology ; Cell Differentiation/immunology ; DNA (Cytosine-5-)-Methyltransferase 1/genetics ; DNA (Cytosine-5-)-Methyltransferase 1/metabolism ; DNA Methylation/genetics ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Gene Expression Profiling ; Hematopoietic Stem Cells/cytology ; Homeostasis/immunology ; Lupus Erythematosus, Systemic/immunology ; Mice ; Mice, Knockout
    Chemical Substances DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37)
    Language English
    Publishing date 2021-12-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2100624
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The yin and yang of microglia.

    Czeh, Melinda / Gressens, Pierre / Kaindl, Angela M

    Developmental neuroscience

    2011  Volume 33, Issue 3-4, Page(s) 199–209

    Abstract: Microglia, the resident immune cells of the mammalian central nervous system (CNS), play a pivotal role in both physiological and pathological conditions such as the restoration of CNS integrity and the progression of neurodegenerative disorders. ... ...

    Abstract Microglia, the resident immune cells of the mammalian central nervous system (CNS), play a pivotal role in both physiological and pathological conditions such as the restoration of CNS integrity and the progression of neurodegenerative disorders. Extensive data have been published that describe neuroinflammation by microglial activation to have detrimental consequences on the developing and mature brain. On the other hand, a properly directed and limited inflammatory response is known to be a natural healing process after an insult in several other tissues. Thus, it is not surprising that research results illustrating benefits of neuroinflammation have been emerging over the past decade. Inflammation-mediated benefits for CNS outcomes include mechanisms such as neuroprotection, mobilization of neural precursors for repair, remyelination and axonal regeneration. Here, we review data that highlight the dual aspects of microglia with a focus on the developing brain, i.e. as aggressors potentiating damage and as helpers in the recovery process following CNS damage.
    MeSH term(s) Aging/physiology ; Brain/cytology ; Brain/embryology ; Brain/growth & development ; Brain/pathology ; Central Nervous System/cytology ; Central Nervous System/immunology ; Central Nervous System/pathology ; Central Nervous System/physiology ; Encephalitis/immunology ; Encephalitis/pathology ; Humans ; Microglia/cytology ; Microglia/physiology ; Nerve Degeneration/pathology ; Nerve Degeneration/physiopathology
    Language English
    Publishing date 2011
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 556887-0
    ISSN 1421-9859 ; 0378-5866
    ISSN (online) 1421-9859
    ISSN 0378-5866
    DOI 10.1159/000328989
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The Yin and Yang of Microglia

    Czeh, Melinda / Gressens, Pierre / Kaindl, Angela M.

    Developmental Neuroscience

    2011  Volume 33, Issue 3-4, Page(s) 199–209

    Abstract: Microglia, the resident immune cells of the mammalian central nervous system (CNS), play a pivotal role in both physiological and pathological conditions such as the restoration of CNS integrity and the progression of neurodegenerative disorders. ... ...

    Institution Department of Pediatric Neurology, Campus Virchow-Klinikum, and Institute of Neuroanatomy and Cell Biology, Campus Mitte, Charité – Universitätsmedizin Berlin, Berlin, Germany Inserm U676 Faculté de Médecine Denis Diderot, Université Paris 7 Service de Neurologie Pédiatrique, Hôpital Robert Debré, AP HP, and PremUP, Paris, France
    Abstract Microglia, the resident immune cells of the mammalian central nervous system (CNS), play a pivotal role in both physiological and pathological conditions such as the restoration of CNS integrity and the progression of neurodegenerative disorders. Extensive data have been published that describe neuroinflammation by microglial activation to have detrimental consequences on the developing and mature brain. On the other hand, a properly directed and limited inflammatory response is known to be a natural healing process after an insult in several other tissues. Thus, it is not surprising that research results illustrating benefits of neuroinflammation have been emerging over the past decade. Inflammation-mediated benefits for CNS outcomes include mechanisms such as neuroprotection, mobilization of neural precursors for repair, remyelination and axonal regeneration. Here, we review data that highlight the dual aspects of microglia with a focus on the developing brain, i.e. as aggressors potentiating damage and as helpers in the recovery process following CNS damage.
    Keywords Microglia ; Brain ; Neurodegeneration ; Neuroprotection ; Inflammation
    Language English
    Publishing date 2011-07-15
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Review
    ZDB-ID 556887-0
    ISBN 978-3-8055-9884-2 ; 978-3-8055-9885-9 ; 3-8055-9884-X ; 3-8055-9885-8
    ISSN 1421-9859 ; 0378-5866
    ISSN (online) 1421-9859
    ISSN 0378-5866
    DOI 10.1159/000328989
    Database Karger publisher's database

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  6. Article ; Online: Visualizing the dynamic of adoptively transferred T cells during the rejection of large established tumors.

    Charo, Jehad / Perez, Cynthia / Buschow, Christian / Jukica, Ana / Czeh, Melinda / Blankenstein, Thomas

    European journal of immunology

    2011  Volume 41, Issue 11, Page(s) 3187–3197

    Abstract: Adoptive T-cell therapy (ATCT) can result in tumor rejection, yet the behavior and fate of the introduced T cells remain unclear. We developed a novel bioluminescence mouse model, which enabled highly sensitive detection of T-cell signals at the single- ... ...

    Abstract Adoptive T-cell therapy (ATCT) can result in tumor rejection, yet the behavior and fate of the introduced T cells remain unclear. We developed a novel bioluminescence mouse model, which enabled highly sensitive detection of T-cell signals at the single-cell level. Transferred T cells preferentially accumulated within antigen-positive tumors, relative to the unaffected areas in each mouse, and remarkably, expanded within both lymphopenic and P14 mice. This expansion was controlled and efficient, as evaluated by bioluminescence imaging (BLI) of the T-cell signals and by tumor rejection respectively. Analysis of the population dynamics of transferred T cells in ATCT of large tumors revealed that proliferation did not always follow a simple linear pattern of expansion, but showed an oscillating pattern of expansion and contraction that was often followed by a rebound, until full tumor rejection was achieved. Furthermore, visualizing the recall response showed that the transferred T cells responded expeditiously, indicating the ability of these cells to survive, establish memory and compete with endogenous T cells for as long as 1 year after rejecting the tumor.
    MeSH term(s) Adoptive Transfer/methods ; Animals ; Cell Separation ; Cell Transplantation/methods ; Chemotaxis, Leukocyte/immunology ; Female ; Flow Cytometry ; Immunotherapy, Adoptive/methods ; Luciferases, Renilla/genetics ; Luminescent Measurements ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasms, Experimental/immunology ; T-Lymphocytes/transplantation
    Chemical Substances Luciferases, Renilla (EC 1.13.12.5)
    Language English
    Publishing date 2011-11
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.201141452
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 85: Show issues

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  7. Article ; Online: Immunogenicity of premalignant lesions is the primary cause of general cytotoxic T lymphocyte unresponsiveness.

    Willimsky, Gerald / Czéh, Melinda / Loddenkemper, Christoph / Gellermann, Johanna / Schmidt, Karin / Wust, Peter / Stein, Harald / Blankenstein, Thomas

    The Journal of experimental medicine

    2008  Volume 205, Issue 7, Page(s) 1687–1700

    Abstract: Cancer is sporadic in nature, characterized by an initial clonal oncogenic event and usually a long latency. When and how it subverts the immune system is unknown. We show, in a model of sporadic immunogenic cancer, that tumor-specific tolerance closely ... ...

    Abstract Cancer is sporadic in nature, characterized by an initial clonal oncogenic event and usually a long latency. When and how it subverts the immune system is unknown. We show, in a model of sporadic immunogenic cancer, that tumor-specific tolerance closely coincides with the first tumor antigen recognition by B cells. During the subsequent latency period until tumors progress, the mice acquire general cytotoxic T lymphocyte (CTL) unresponsiveness, which is associated with high transforming growth factor (TGF) beta1 levels and expansion of immature myeloid cells (iMCs). In mice with large nonimmunogenic tumors, iMCs expand but TGF-beta1 serum levels are normal, and unrelated CTL responses are undiminished. We conclude that (a) tolerance to the tumor antigen occurs at the premalignant stage, (b) tumor latency is unlikely caused by CTL control, and (c) a persistent immunogenic tumor antigen causes general CTL unresponsiveness but tumor burden and iMCs per se do not.
    MeSH term(s) Animals ; Antigens, Neoplasm/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Immune Tolerance ; Mice ; Mice, Knockout ; Neoplasms/immunology ; Neoplasms/pathology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/pathology ; Transforming Growth Factor beta1/immunology
    Chemical Substances Antigens, Neoplasm ; Transforming Growth Factor beta1
    Language English
    Publishing date 2008-06-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20072016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Myeloid leukemia with transdifferentiation plasticity developing from T-cell progenitors.

    Riemke, Pia / Czeh, Melinda / Fischer, Josephine / Walter, Carolin / Ghani, Saeed / Zepper, Matthias / Agelopoulos, Konstantin / Lettermann, Stephanie / Gebhardt, Marie L / Mah, Nancy / Weilemann, Andre / Grau, Michael / Gröning, Verena / Haferlach, Torsten / Lenze, Dido / Delwel, Ruud / Prinz, Marco / Andrade-Navarro, Miguel A / Lenz, Georg /
    Dugas, Martin / Müller-Tidow, Carsten / Rosenbauer, Frank

    The EMBO journal

    2016  Volume 35, Issue 22, Page(s) 2399–2416

    Abstract: Unfavorable patient survival coincides with lineage plasticity observed in human acute leukemias. These cases are assumed to arise from hematopoietic stem cells, which have stable multipotent differentiation potential. However, here we report that ... ...

    Abstract Unfavorable patient survival coincides with lineage plasticity observed in human acute leukemias. These cases are assumed to arise from hematopoietic stem cells, which have stable multipotent differentiation potential. However, here we report that plasticity in leukemia can result from instable lineage identity states inherited from differentiating progenitor cells. Using mice with enhanced c-Myc expression, we show, at the single-cell level, that T-lymphoid progenitors retain broad malignant lineage potential with a high capacity to differentiate into myeloid leukemia. These T-cell-derived myeloid blasts retain expression of a defined set of T-cell transcription factors, creating a lymphoid epigenetic memory that confers growth and propagates myeloid/T-lymphoid plasticity. Based on these characteristics, we identified a correlating human leukemia cohort and revealed targeting of Jak2/Stat3 signaling as a therapeutic possibility. Collectively, our study suggests the thymus as a source for myeloid leukemia and proposes leukemic plasticity as a driving mechanism. Moreover, our results reveal a pathway-directed therapy option against thymus-derived myeloid leukemogenesis and propose a model in which dynamic progenitor differentiation states shape unique neoplastic identities and therapy responses.
    MeSH term(s) Animals ; Cell Transdifferentiation ; Humans ; Leukemia, Myeloid/pathology ; Lymphoid Progenitor Cells/physiology ; Mice ; T-Lymphocytes/physiology
    Language English
    Publishing date 2016-08-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.15252/embj.201693927
    Database MEDical Literature Analysis and Retrieval System OnLINE

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