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Your search keyword '"Schneider, Matthias M [0000-0002-1894-1859]"' showing total 3 results
Start Over Author "Schneider, Matthias M [0000-0002-1894-1859]" Topic biology
3 results on '"Schneider, Matthias M [0000-0002-1894-1859]"'

1. Microfluidic Antibody Affinity Profiling Reveals the Role of Memory Reactivation and Cross-Reactivity in the Defense Against SARS-CoV-2

Author

Denninger, Viola, Xu, Catherine K, Meisl, Georg, Morgunov, Alexey S, Fiedler, Sebastian, Ilsley, Alison, Emmenegger, Marc, Malik, Anisa Y, Piziorska, Monika A, Schneider, Matthias M, Devenish, Sean R A, Kosmoliaptsis, Vasilis, Aguzzi, Adriano, Fiegler, Heike, Knowles, Tuomas P J, Denninger, Viola [0000-0001-9770-8723], Xu, Catherine K [0000-0003-4726-636X], Meisl, Georg [0000-0002-6562-7715], Fiedler, Sebastian [0000-0003-0953-4327], Schneider, Matthias M [0000-0002-1894-1859], Knowles, Tuomas PJ [0000-0002-7879-0140], Apollo - University of Cambridge Repository, University of Zurich, and Knowles, Tuomas P J

Subjects
cross-reactivity, SARS-CoV-2, antibody affinity, Microfluidics, 10208 Institute of Neuropathology, virus diseases, COVID-19, 610 Medicine & health, 2725 Infectious Diseases, Antibodies, Viral, Infectious Diseases, Spike Glycoprotein, Coronavirus, 570 Life sciences, biology, antibody concentration, antibody profiling, Humans
Abstract

Funder: Universit?tsspital Z?rich, Funder: Biotechnology and Biological Sciences Research Council, Funder: NOMIS Stiftung, Funder: Universit?t Z?rich, Recent efforts in understanding the course and severity of SARS-CoV-2 infections have highlighted both potentially beneficial and detrimental effects of cross-reactive antibodies derived from memory immunity. Specifically, due to a significant degree of sequence similarity between SARS-CoV-2 and other members of the coronavirus family, memory B-cells that emerged from previous infections with endemic human coronaviruses (HCoVs) could be reactivated upon encountering the newly emerged SARS-CoV-2, thus prompting the production of cross-reactive antibodies. Determining the affinity and concentration of these potentially cross-reactive antibodies to the new SARS-CoV-2 antigens is therefore particularly important when assessing both existing immunity against common HCoVs and adverse effects like antibody-dependent enhancement (ADE) in COVID-19. However, these two fundamental parameters cannot easily be disentangled by surface-based assays like enzyme-linked immunosorbent assays (ELISAs), which are routinely used to assess cross-reactivity. Here, we have used microfluidic antibody affinity profiling (MAAP) to quantitatively evaluate the humoral immune response in COVID-19 convalescent patients by determining both antibody affinity and concentration against spike antigens of SARS-CoV-2 directly in nine convalescent COVID-19 patient and three pre-pandemic sera that were seropositive for common HCoVs. All 12 sera contained low concentrations of high-affinity antibodies against spike antigens of HCoV-NL63 and HCoV-HKU1, indicative of past exposure to these pathogens, while the affinity against the SARS-CoV-2 spike protein was lower. These results suggest that cross-reactivity as a consequence of memory reactivation upon an acute SARS-CoV-2 infection may not be a significant factor in generating immunity against SARS-CoV-2.

Published
2022

2. LAG3 is not expressed in human and murine neurons and does not modulate α‐synucleinopathies

Author

Emmenegger, Marc, De Cecco, Elena, Hruska-Plochan, Marian, Eninger, Timo, Schneider, Matthias M, Barth, Melanie, Tantardini, Elena, De Rossi, Pierre, Bacioglu, Mehtap, Langston, Rebekah G, Kaganovich, Alice, Bengoa-Vergniory, Nora, Gonzalez-Guerra, Andrès, Avar, Merve, Heinzer, Daniel, Reimann, Regina, Häsler, Lisa M, Herling, Therese W, Matharu, Naunehal S, Landeck, Natalie, Luk, Kelvin, Melki, Ronald, Kahle, Philipp J, Hornemann, Simone, Knowles, Tuomas PJ, Cookson, Mark R, Polymenidou, Magdalini, Jucker, Mathias, Aguzzi, Adriano, Universität Zürich [Zürich] = University of Zurich (UZH), German Research Center for Neurodegenerative Diseases - Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), University of Cambridge [UK] (CAM), National Institutes of Health [Bethesda] (NIH), University of Oxford [Oxford], Penn Cardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, Laboratoire des Maladies Neurodégénératives - UMR 9199 (LMN), Centre National de la Recherche Scientifique (CNRS)-Service MIRCEN (MIRCEN), Institut de Biologie François JACOB (JACOB), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, University of Tübingen, National Centre for Competence in Research (NCCR) RNA & Disease (51NF40-182880), European Project: 670958,H2020,ERC-2014-ADG,PRION2020(2015), European Project: 674979,H2020,H2020-MSCA-ITN-2015,NANOTRANS(2016), European Project: (grant No 116060),IMPRiND, University of Oxford, Service MIRCEN (MIRCEN), Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Emmenegger, Marc [0000-0002-6073-8811], De Cecco, Elena [0000-0002-0148-2596], Hruska-Plochan, Marian [0000-0002-9253-4362], Schneider, Matthias M [0000-0002-1894-1859], Tantardini, Elena [0000-0001-9189-3390], Bacioglu, Mehtap [0000-0003-0304-7026], Bengoa-Vergniory, Nora [0000-0002-3700-0464], Avar, Merve [0000-0003-4665-5558], Heinzer, Daniel [0000-0002-3282-4042], Landeck, Natalie [0000-0002-8399-4009], Luk, Kelvin [0000-0002-6591-6269], Melki, Ronald [0000-0003-0000-7096], Hornemann, Simone [0000-0002-2674-9891], Cookson, Mark R [0000-0002-1058-3831], Jucker, Mathias [0000-0001-9045-1072], Aguzzi, Adriano [0000-0002-0344-6708], Apollo - University of Cambridge Repository, Hruska‐Plochan, Marian [0000-0002-9253-4362], Bengoa‐Vergniory, Nora [0000-0002-3700-0464], University of Zurich, and Aguzzi, Adriano

Subjects
Medicine (General), prionoids, Synucleinopathies, 10208 Institute of Neuropathology, 610 Medicine & health, Mice, Transgenic, QH426-470, Article, Mice, R5-920, α-synuclein, Genetics, Animals, Humans, ddc:610, Neurons, α‐synuclein, neurodegeneration, Parkinson Disease, Articles, nervous system diseases, EMBO27, 1313 Molecular Medicine, genetics [alpha-Synuclein], alpha-Synuclein, 570 Life sciences, biology, Molecular Medicine, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], 11493 Department of Quantitative Biomedicine, Neuroscience, LAG3
Abstract

Funder: University of Zurich and University Hospital of Zurich, Funder: NOMIS Stiftung (NOMIS Foundation); Id: http://dx.doi.org/10.13039/501100008483, Funder: Forschungskredit University of Zurich, While the initial pathology of Parkinson’s disease and other α‐synucleinopathies is often confined to circumscribed brain regions, it can spread and progressively affect adjacent and distant brain locales. This process may be controlled by cellular receptors of α‐synuclein fibrils, one of which was proposed to be the LAG3 immune checkpoint molecule. Here, we analysed the expression pattern of LAG3 in human and mouse brains. Using a variety of methods and model systems, we found no evidence for LAG3 expression by neurons. While we confirmed that LAG3 interacts with α‐synuclein fibrils, the specificity of this interaction appears limited. Moreover, overexpression of LAG3 in cultured human neural cells did not cause any worsening of α‐synuclein pathology ex vivo. The overall survival of A53T α‐synuclein transgenic mice was unaffected by LAG3 depletion, and the seeded induction of α‐synuclein lesions in hippocampal slice cultures was unaffected by LAG3 knockout. These data suggest that the proposed role of LAG3 in the spreading of α‐synucleinopathies is not universally valid.

Published
2021
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3. Microfluidic characterisation reveals broad range of SARS-CoV-2 antibody affinity in human plasma

Author

Raphael P. B. Jacquat, Matthias Schneider, Alison Ilsley, Itzel Condado Morales, Heike Fiegler, Catherine K. Xu, Tuomas P. J. Knowles, Chryssa Zografou, Georg Meisl, Didier Trono, Marc Emmenegger, Viola Denninger, Vasilis Kosmoliaptsis, Adriano Aguzzi, Manuela R Zimmermann, Lidia Madrigal, Sebastian Fiedler, Priscilla Turelli, Beat M. Frey, University of Zurich, Schneider, Matthias M [0000-0002-1894-1859], Emmenegger, Marc [0000-0002-6073-8811], Condado Morales, Itzel [0000-0001-7592-4556], Turelli, Priscilla [0000-0002-7302-9977], Zografou, Chryssa [0000-0002-2934-2739], Zimmermann, Manuela R [0000-0002-3443-2050], Frey, Beat M [0000-0002-2514-8621], Fiedler, Sebastian [0000-0003-0953-4327], Jacquat, Raphaël Pb [0000-0002-8661-9722], Ilsley, Alison [0000-0003-1772-6951], Kosmoliaptsis, Vasilis [0000-0001-7298-1387], Trono, Didier [0000-0002-3383-0401], Aguzzi, Adriano [0000-0002-0344-6708], and Apollo - University of Cambridge Repository

Subjects
Adult, Male, Health, Toxicology and Mutagenesis, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), monoclonal-antibodies, Microfluidics, 10208 Institute of Neuropathology, Antibody Affinity, 610 Medicine & health, Genetics and Molecular Biology (miscellaneous), binding-affinity, Plant Science, Cross Reactions, Antibodies, Viral, Biochemistry, Severity of Illness Index, Biochemistry, Genetics and Molecular Biology (miscellaneous), Neutralization, generation, Humans, Toxicology and Mutagenesis, Receptor, Research Articles, COVID, Aged, Cytopathic effect, B-Lymphocytes, Ecology, biology, SARS-CoV-2, Chemistry, COVID-19, Middle Aged, Surface Plasmon Resonance, Virology, Orders of magnitude (mass), Dissociation constant, Health, Polyclonal antibodies, Spike Glycoprotein, Coronavirus, biology.protein, 570 Life sciences, Female, Angiotensin-Converting Enzyme 2, Antibody, Research Article
Abstract

Funder: Herchel Smith Fund, Funder: St John’s College Cambridge, Funder: Centre for Misfolding Diseases, Cambridge, Funder: Swiss FCS and the Forschungskredit of the University of Zurich, Funder: Frances and Augustus Newman Foundation, Funder: BBRSC, Funder: NOMIS Foundation, The clinical outcome of SARS-CoV-2 infections, which can range from asymptomatic to lethal, is crucially shaped by the concentration of antiviral antibodies and by their affinity to their targets. However, the affinity of polyclonal antibody responses in plasma is difficult to measure. Here we used microfluidic antibody affinity profiling (MAAP) to determine the aggregate affinities and concentrations of anti-SARS-CoV-2 antibodies in plasma samples of 42 seropositive individuals, 19 of which were healthy donors, 20 displayed mild symptoms, and 3 were critically ill. We found that dissociation constants, K d, of anti-receptor-binding domain antibodies spanned 2.5 orders of magnitude from sub-nanomolar to 43 nM. Using MAAP we found that antibodies of seropositive individuals induced the dissociation of pre-formed spike-ACE2 receptor complexes, which indicates that MAAP can be adapted as a complementary receptor competition assay. By comparison with cytopathic effect-based neutralisation assays, we show that MAAP can reliably predict the cellular neutralisation ability of sera, which may be an important consideration when selecting the most effective samples for therapeutic plasmapheresis and tracking the success of vaccinations.

Published
2021
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