dc.date.accessioned | 2020-02-10T19:06:30Z | |
dc.date.available | 2020-02-10T19:06:30Z | |
dc.date.created | 2019-01-18T09:33:40Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Cabral-Marques, Otavio Marques, Alexandre Melvær, Giil Lasse De Vito, Roberta Rademacher, Judith Günther, Jeannine Lange, Tanja Humrich, Jens Klapa, Sebastian Schinke, Susanne Schimke, Lena Marschner, Gabriele Pitann, Silke Adler, Sabine Dechend, Ralf Muller, Dominik N. Braicu, Ioana Sehouli, Jalid Schulze-Forster, Kai Trippel, Tobias Scheibenbogen, Carmen Staff, Anne Cathrine Mertens, Peter Löbel, Madlen Mastroianni, Justin Plattfaut, Corinna Gieseler, Frank Dragun, Duska Engelhardt, Barbara Elizabeth Fernandez-Cabezudo, Maria Ochs, Hans D Al-Ramadi, Basel K Lamprecht, Peter Mueller, Antje Heidecke, Harald Riemekasten, Gabriela . GPCR-specific autoantibody signatures are associated with physiological and pathological immune homeostasis. Nature Communications. 2018, 9 | |
dc.identifier.uri | http://hdl.handle.net/10852/72928 | |
dc.description.abstract | Autoantibodies have been associated with autoimmune diseases. However, studies have identified autoantibodies in healthy donors (HD) who do not develop autoimmune disorders. Here we provide evidence of a network of immunoglobulin G (IgG) autoantibodies targeting G protein-coupled receptors (GPCR) in HD compared to patients with systemic sclerosis, Alzheimer’s disease, and ovarian cancer. Sex, age and pathological conditions affect autoantibody correlation and hierarchical clustering signatures, yet many of the correlations are shared across all groups, indicating alterations to homeostasis. Furthermore, we identify relationships between autoantibodies targeting structurally and functionally related molecules, such as vascular, neuronal or chemokine receptors. Finally, autoantibodies targeting the endothelin receptor type A (EDNRA) exhibit chemotactic activity, as demonstrated by neutrophil migration toward HD-IgG in an EDNRA-dependent manner and in the direction of IgG from EDNRA-immunized mice. Our data characterizing the in vivo signatures of anti-GPCR autoantibodies thus suggest that they are a physiological part of the immune system. | en_US |
dc.language | EN | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.title | GPCR-specific autoantibody signatures are associated with physiological and pathological immune homeostasis | en_US |
dc.type | Journal article | en_US |
dc.creator.author | Cabral-Marques, Otavio | |
dc.creator.author | Marques, Alexandre | |
dc.creator.author | Melvær, Giil Lasse | |
dc.creator.author | De Vito, Roberta | |
dc.creator.author | Rademacher, Judith | |
dc.creator.author | Günther, Jeannine | |
dc.creator.author | Lange, Tanja | |
dc.creator.author | Humrich, Jens | |
dc.creator.author | Klapa, Sebastian | |
dc.creator.author | Schinke, Susanne | |
dc.creator.author | Schimke, Lena | |
dc.creator.author | Marschner, Gabriele | |
dc.creator.author | Pitann, Silke | |
dc.creator.author | Adler, Sabine | |
dc.creator.author | Dechend, Ralf | |
dc.creator.author | Muller, Dominik N. | |
dc.creator.author | Braicu, Ioana | |
dc.creator.author | Sehouli, Jalid | |
dc.creator.author | Schulze-Forster, Kai | |
dc.creator.author | Trippel, Tobias | |
dc.creator.author | Scheibenbogen, Carmen | |
dc.creator.author | Staff, Anne Cathrine | |
dc.creator.author | Mertens, Peter | |
dc.creator.author | Löbel, Madlen | |
dc.creator.author | Mastroianni, Justin | |
dc.creator.author | Plattfaut, Corinna | |
dc.creator.author | Gieseler, Frank | |
dc.creator.author | Dragun, Duska | |
dc.creator.author | Engelhardt, Barbara Elizabeth | |
dc.creator.author | Fernandez-Cabezudo, Maria | |
dc.creator.author | Ochs, Hans D | |
dc.creator.author | Al-Ramadi, Basel K | |
dc.creator.author | Lamprecht, Peter | |
dc.creator.author | Mueller, Antje | |
dc.creator.author | Heidecke, Harald | |
dc.creator.author | Riemekasten, Gabriela | |
cristin.unitcode | 185,53,45,0 | |
cristin.unitname | Kvinneklinikken | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 2 | |
dc.identifier.cristin | 1659931 | |
dc.identifier.bibliographiccitation | info:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Nature Communications&rft.volume=9&rft.spage=&rft.date=2018 | |
dc.identifier.jtitle | Nature Communications | |
dc.identifier.volume | 9 | |
dc.identifier.issue | 1 | |
dc.identifier.doi | https://doi.org/10.1038/s41467-018-07598-9 | |
dc.identifier.urn | URN:NBN:no-76082 | |
dc.type.document | Tidsskriftartikkel | en_US |
dc.type.peerreviewed | Peer reviewed | |
dc.source.issn | 2041-1723 | |
dc.identifier.fulltext | Fulltext https://www.duo.uio.no/bitstream/handle/10852/72928/2/Cabral_Marques_et_al_2018.pdf | |
dc.type.version | PublishedVersion | |
cristin.articleid | 5224 | |