Renner, Kerstin and Neumayer, Sophia and Talke, Yvonne and Buchtler, Simone and Schmidbauer, Kathrin and Nimmerjahn, Falk and Lux, Anja and Winter, Frederike and Salewski, Jan-Nicklas and Mack, Matthias (2022) B-cell modulation with anti-CD79b antibodies ameliorates experimental autoimmune encephalitis in mice. EUROPEAN JOURNAL OF IMMUNOLOGY, 52 (4). pp. 656-668. ISSN 0014-2980, 1521-4141
Full text not available from this repository. (Request a copy)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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | T-CELLS; MULTIPLE-SCLEROSIS; ANTIGEN RECEPTOR; CROSS-LINKING; BETA; DEPLETION; DISEASE; CD79B; LYMPHOCYTES; RITUXIMAB; autoimmunity; B cells; neuroimmunology |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II Medicine > Zentren des Universitätsklinikums Regensburg > Regensburger Centrum für Interventionelle Immunologie (RCI) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 14 Nov 2023 13:14 |
| Last Modified: | 14 Nov 2023 13:14 |
| URI: | https://pred.uni-regensburg.de/id/eprint/56731 |
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