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  1. Article ; Online: Donor-But Not Recipient-Derived Cells Produce Collagen-1 in Chronically Rejected Cardiac Allografts.

    Balam, Saidou / Buchtler, Simone / Winter, Frederike / Schmidbauer, Kathrin / Neumayer, Sophia / Talke, Yvonne / Renner, Kerstin / Geissler, Edward K / Mack, Matthias

    Frontiers in immunology

    2022  Volume 12, Page(s) 816509

    Abstract: Fibrosis is a prominent feature of chronic allograft rejection, caused by an excessive production of matrix proteins, including collagen-1. Several cell types produce collagen-1, including mesenchymal fibroblasts and cells of hematopoietic origin. Here, ... ...

    Abstract Fibrosis is a prominent feature of chronic allograft rejection, caused by an excessive production of matrix proteins, including collagen-1. Several cell types produce collagen-1, including mesenchymal fibroblasts and cells of hematopoietic origin. Here, we sought to determine whether tissue-resident donor-derived cells or allograft-infiltrating recipient-derived cells are responsible for allograft fibrosis, and whether hematopoietic cells contribute to collagen production. A fully MHC-mismatched mouse heterotopic heart transplantation model was used, with transient depletion of CD4
    MeSH term(s) Animals ; Biomarkers ; Chronic Disease ; Collagen Type I/biosynthesis ; Collagen Type I/immunology ; Disease Models, Animal ; Disease Susceptibility ; Graft Rejection/diagnosis ; Graft Rejection/etiology ; Graft Rejection/metabolism ; Heart Transplantation/adverse effects ; Heart Transplantation/methods ; Immunophenotyping ; Mice ; Mice, Transgenic ; Tissue Donors ; Transplantation, Homologous
    Chemical Substances Biomarkers ; Collagen Type I
    Language English
    Publishing date 2022-01-19
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.816509
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: B-cell modulation with anti-CD79b antibodies ameliorates experimental autoimmune encephalitis in mice.

    Renner, Kerstin / Neumayer, Sophia / Talke, Yvonne / Buchtler, Simone / Schmidbauer, Kathrin / Nimmerjahn, Falk / Lux, Anja / Winter, Frederike / Salewski, Jan-Nicklas / Mack, Matthias

    European journal of immunology

    2022  Volume 52, Issue 4, Page(s) 656–668

    Abstract: B cells play a major role in the pathogenesis of many autoimmune diseases like MS, rheumatoid arthritis, or systemic lupus erythematosus. Depletion of B cells with anti-CD20 antibodies is an established therapy for MS. However, total B-cell depletion ... ...

    Abstract B cells play a major role in the pathogenesis of many autoimmune diseases like MS, rheumatoid arthritis, or systemic lupus erythematosus. Depletion of B cells with anti-CD20 antibodies is an established therapy for MS. However, total B-cell depletion will also affect regulatory B cells that are known to suppress autoimmune responses. In our studies, we describe an alternative approach based on targeting CD79b that induces only partial B-cell depletion and achieves therapeutic effects by B-cell modulation. Prophylactic and therapeutic treatment with an antibody against CD79b and also a deglycosylated variant of this antibody, lacking effector function like antibody-dependent cellular cytotoxicity or complement activation, significantly reduced the development and progression of EAE in mice. Our data show that modulation of B cells via CD79b is equally effective as almost complete B-cell depletion with anti-CD20 antibodies and may constitute an alternative approach to treat MS.
    MeSH term(s) Animals ; Antibodies ; Antigens, CD20 ; Autoimmune Diseases ; Autoimmunity ; B-Lymphocytes ; Encephalitis/drug therapy ; Encephalitis/pathology ; Mice
    Chemical Substances Antibodies ; Antigens, CD20
    Language English
    Publishing date 2022-01-11
    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.202149523
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Expression of IL-3 receptors and impact of IL-3 on human T and B cells.

    Renner, Kerstin / Metz, Sophia / Metzger, Anne-Mieke / Neumayer, Sophia / Schmidbauer, Kathrin / Talke, Yvonne / Buchtler, Simone / Halbritter, Dagmar / Mack, Matthias

    Cellular immunology

    2018  Volume 334, Page(s) 49–60

    Abstract: A large number of animal models revealed that IL-3 plays an important role for the development of T and B cell-mediated autoimmune diseases. However, little is known about the expression and regulation of IL-3 receptors in human T and B cells and how IL- ... ...

    Abstract A large number of animal models revealed that IL-3 plays an important role for the development of T and B cell-mediated autoimmune diseases. However, little is known about the expression and regulation of IL-3 receptors in human T and B cells and how IL-3 modulates the activation and survival of these cells. We show that the IL-3 receptor CD123 is substantially upregulated on proliferating CD4
    MeSH term(s) Autoimmune Diseases/immunology ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cytokines/immunology ; Humans ; Interleukin-3/immunology ; Interleukin-3 Receptor alpha Subunit/immunology ; Lymphocyte Activation/immunology ; Receptors, Interleukin-3/immunology ; Up-Regulation/immunology
    Chemical Substances Cytokines ; IL3 protein, human ; Interleukin-3 ; Interleukin-3 Receptor alpha Subunit ; Receptors, Interleukin-3
    Language English
    Publishing date 2018-09-26
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80094-6
    ISSN 1090-2163 ; 0008-8749
    ISSN (online) 1090-2163
    ISSN 0008-8749
    DOI 10.1016/j.cellimm.2018.09.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: IL-3 Triggers Chronic Rejection of Cardiac Allografts by Activation of Infiltrating Basophils.

    Balam, Saidou / Schiechl-Brachner, Gabriela / Buchtler, Simone / Halbritter, Dagmar / Schmidbauer, Kathrin / Talke, Yvonne / Neumayer, Sophia / Salewski, Jan-Niklas / Winter, Frederike / Karasuyama, Hajime / Yamanishi, Yoshinori / Renner, Kerstin / Geissler, Edward K / Mack, Matthias

    Journal of immunology (Baltimore, Md. : 1950)

    2019  Volume 202, Issue 12, Page(s) 3514–3523

    Abstract: Chronic rejection is a major problem in transplantation medicine, largely resistant to therapy, and poorly understood. We have shown previously that basophil-derived IL-4 contributes to fibrosis and vasculopathy in a model of heart transplantation with ... ...

    Abstract Chronic rejection is a major problem in transplantation medicine, largely resistant to therapy, and poorly understood. We have shown previously that basophil-derived IL-4 contributes to fibrosis and vasculopathy in a model of heart transplantation with depletion of CD4
    MeSH term(s) Animals ; Basophils/immunology ; Cell Movement ; Cells, Cultured ; Chronic Disease ; Disease Models, Animal ; Graft Rejection/immunology ; Heart Transplantation ; Humans ; Interleukin-3/genetics ; Interleukin-3/metabolism ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Transplantation, Homologous ; Up-Regulation
    Chemical Substances Interleukin-3 ; Interleukin-6
    Language English
    Publishing date 2019-05-08
    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.1801269
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Cellular Origin and Functional Relevance of Collagen I Production in the Kidney.

    Buchtler, Simone / Grill, Alexandra / Hofmarksrichter, Stefanie / Stöckert, Petra / Schiechl-Brachner, Gabriela / Rodriguez Gomez, Manuel / Neumayer, Sophia / Schmidbauer, Kathrin / Talke, Yvonne / Klinkhammer, Barbara M / Boor, Peter / Medvinsky, Alexander / Renner, Kerstin / Castrop, Hayo / Mack, Matthias

    Journal of the American Society of Nephrology : JASN

    2018  Volume 29, Issue 7, Page(s) 1859–1873

    Abstract: ... ...

    Abstract Background
    MeSH term(s) Acute Kidney Injury/etiology ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Acute Kidney Injury/physiopathology ; Adenine ; Animals ; Bone Marrow Cells/metabolism ; Cell Lineage ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Epithelial Cells/metabolism ; Female ; Fibroblasts/metabolism ; Fibrosis ; Glomerular Filtration Rate ; Hematopoiesis ; Kidney/pathology ; Kidney/physiopathology ; Kidney Tubules/cytology ; Mice ; Mice, Knockout ; Renal Insufficiency, Chronic/chemically induced ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/physiopathology ; Ureteral Obstruction/complications
    Chemical Substances Collagen Type I ; Adenine (JAC85A2161)
    Language English
    Publishing date 2018-05-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2018020138
    Database MEDical Literature Analysis and Retrieval System OnLINE

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