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6 results on '"Cordero-Gómez, César"'

1. Human cerebrospinal fluid monoclonal CASPR2 autoantibodies induce changes in electrophysiology, functional MRI, and behavior in rodent models

Author

van Hoof, Scott, Kreye, Jakob, Cordero-Gómez, César, Hoffmann, Julius, Momsen Reincke, S., Sánchez-Sendin, Elisa, Duong, Sophie L., Upadhya, Manoj, Dhangar, Divya, Michór, Paulina, Woodhall, Gavin L., Küpper, Maraike, Oder, Andreas, Kuchling, Joseph, Koch, Stefan Paul, Mueller, Susanne, Boehm-Sturm, Philipp, von Kries, Jens Peter, Finke, Carsten, Kirschstein, Timo, Wright, Sukhvir K., and Prüss, Harald

Published
2024
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2. KCNA2 IgG autoimmunity in neuropsychiatric diseases

Author

Arlt, Friederike A., Miske, Ramona, Machule, Marie-Luise, Broegger Christensen, Peter, Mindorf, Swantje, Teegen, Bianca, Borowski, Kathrin, Buthut, Maria, Rößling, Rosa, Sánchez-Sendín, Elisa, van Hoof, Scott, Cordero-Gómez, César, Bünger, Isabel, Radbruch, Helena, Kraft, Andrea, Ayzenberg, Ilya, Klausewitz, Jaqueline, Hansen, Niels, Timäus, Charles, Körtvelyessy, Peter, Postert, Thomas, Baur-Seack, Kirsten, Rost, Constanze, Brunkhorst, Robert, Doppler, Kathrin, Haigis, Niklas, Hamann, Gerhard, Kunze, Albrecht, Stützer, Alexandra, Maschke, Matthias, Melzer, Nico, Rosenow, Felix, Siebenbrodt, Kai, Stenør, Christian, Dichgans, Martin, Georgakis, Marios K., Fang, Rong, Petzold, Gabor C., Görtler, Michael, Zerr, Inga, Wunderlich, Silke, Mihaljevic, Ivan, Turko, Paul, Schmidt Ettrup, Marianne, Buchholz, Emilie, Foverskov Rasmussen, Helle, Nasouti, Mahoor, Talucci, Ivan, Maric, Hans M., Heinemann, Stefan H., Endres, Matthias, Komorowski, Lars, and Prüss, Harald

Published
2024
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3. Synapsin autoantibodies during pregnancy are associated with fetal abnormalities

Author

Bünger, Isabel, Talucci, Ivan, Kreye, Jakob, Höltje, Markus, Makridis, Konstantin L., Rasmussen, Helle Foverskov, van Hoof, Scott, Cordero-Gomez, César, Ullrich, Tim, Sedlin, Eva, Kreissner, Kai Oliver, Hoffmann, Christian, Milovanovic, Dragomir, Turko, Paul, Paul, Friedemann, Meckies, Jessica, Verlohren, Stefan, Henrich, Wolfgang, Chaoui, Rabih, Maric, Hans Michael, Kaindl, Angela M., and Prüss, Harald

Published
2023
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4. Encephalitis patient-derived monoclonal GABAA receptor antibodies cause epileptic seizures

Author

Kreye, Jakob, Wright, Sukhvir K, van Casteren, Adriana, Stöffler, Laura, Machule, Marie-Luise, Reincke, S Momsen, Nikolaus, Marc, van Hoof, Scott, Sanchez-Sendin, Elisa, Homeyer, Marie A, Cordero Gómez, César, Kornau, Hans-Christian, Schmitz, Dietmar, Kaindl, Angela M, Boehm-Sturm, Philipp, Mueller, Susanne, Wilson, Max A, Upadhya, Manoj A, Dhangar, Divya R, Greenhill, Stuart, Woodhall, Gavin, Turko, Paul, Vida, Imre, Garner, Craig C, Wickel, Jonathan, Geis, Christian, Fukata, Yuko, Fukata, Masaki, Prüss, Harald, Kreye, Jakob, Wright, Sukhvir K, van Casteren, Adriana, Stöffler, Laura, Machule, Marie-Luise, Reincke, S Momsen, Nikolaus, Marc, van Hoof, Scott, Sanchez-Sendin, Elisa, Homeyer, Marie A, Cordero Gómez, César, Kornau, Hans-Christian, Schmitz, Dietmar, Kaindl, Angela M, Boehm-Sturm, Philipp, Mueller, Susanne, Wilson, Max A, Upadhya, Manoj A, Dhangar, Divya R, Greenhill, Stuart, Woodhall, Gavin, Turko, Paul, Vida, Imre, Garner, Craig C, Wickel, Jonathan, Geis, Christian, Fukata, Yuko, Fukata, Masaki, and Prüss, Harald

Abstract

Autoantibodies targeting the GABAA receptor (GABAAR) hallmark an autoimmune encephalitis presenting with frequent seizures and psychomotor abnormalities. Their pathogenic role is still not well-defined, given the common overlap with further autoantibodies and the lack of patient-derived mAbs. Five GABAAR mAbs from cerebrospinal fluid cells bound to various epitopes involving the α1 and γ2 receptor subunits, with variable binding strength and partial competition. mAbs selectively reduced GABAergic currents in neuronal cultures without causing receptor internalization. Cerebroventricular infusion of GABAAR mAbs and Fab fragments into rodents induced a severe phenotype with seizures and increased mortality, reminiscent of encephalitis patients' symptoms. Our results demonstrate direct pathogenicity of autoantibodies on GABAARs independent of Fc-mediated effector functions and provide an animal model for GABAAR encephalitis. They further provide the scientific rationale for clinical treatments using antibody depletion and can serve as tools for the development of antibody-selective immunotherapies.

Published
2021

6. Autoantibody-boosted T-cell reactivation in the target organ triggers manifestation of autoimmune CNS disease.

Author

Flach, Anne-Christine, Litke, Tanja, Strauss, Judith, Haberl, Michael, Cordero Gómez, César, Reindl, Markus, Saiz, Albert, Fehling, Hans-Jörg, Wienands, Jürgen, Odoardi, Francesca, Lühder, Fred, and Flügel, Alexander

Subjects
T cells, AUTOANTIBODIES, GENETICS of autoimmune diseases, GENETICS of multiple sclerosis, CNS demyelinating autoimmune diseases, PHYSIOLOGY
Abstract

Multiple sclerosis (MS) is caused by T cells that are reactive for brain antigens. In experimental autoimmune encephalomyelitis, the animal model for MS, myelin-reactive T cells initiate the autoimmune process when entering the nervous tissue and become reactivated upon local encounter of their cognate CNS antigen. Thereby, the strength of the T-cellular reactivation process within the CNS tissue is crucial for the manifestation and the severity of the clinical disease. Recently, B cells were found to participate in the pathogenesis of CNS autoimmunity, with several diverse underlying mechanisms being under discussion.We here report that B cells play an important role in promoting the initiation process of CNS autoimmunity. Myelin-specific antibodies produced by autoreactive B cells after activation in the periphery diffused into the CNS together with the first invading pathogenic T cells. The antibodies accumulated in resident antigen-presenting phagocytes and significantly enhanced the activation of the incoming effector T cells. The ensuing strong blood-brain barrier disruption and immune cell recruitment resulted in rapid manifestation of clinical disease. Therefore, myelin oligodendrocyte glycoprotein (MOG)-specific autoantibodies can initiate disease bouts by cooperating with the autoreactive T cells in helping them to recognize their autoantigen and become efficiently reactivated within the immune-deprived nervous tissue. [ABSTRACT FROM AUTHOR]

Published
2016
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