TY - JOUR T1 - Increased protease-activated receptor 1 autoantibodies are associated with severe COVID-19 JF - ERJ Open Research JO - erjor DO - 10.1183/23120541.00379-2022 SP - 00379-2022 AU - Florian Tran AU - Danielle MM Harris AU - Alena Scharmacher AU - Hanna Graßhoff AU - Kristina Sterner AU - Susanne Schinke AU - Nadja Käding AU - Jens Y Humrich AU - Otávio Cabral-Marques AU - Joana p Bernardes AU - Neha Mishra AU - Thomas Bahmer AU - Jeanette Franzenburg AU - Bimba F Hoyer AU - Andreas Glück AU - Martina Guggeis AU - Alexander Ossysek AU - Andre Küller AU - Derk Frank AU - Christoph Lange AU - Jan Rupp AU - Jan Heyckendorf AU - Karoline I Gaede AU - Howard Amital AU - Philip Rosenstiel AU - Yehuda Shoenfeld AU - Gilad Halpert AU - Avi Z Rosenberg AU - Kai Schulze-Forster AU - Harald Heidecke AU - Gabriela Riemekasten AU - Stefan Schreiber Y1 - 2022/01/01 UR - http://openres.ersjournals.com/content/early/2022/08/11/23120541.00379-2022.abstract N2 - Immune perturbation is a hallmark of Coronavirus Disease 2019 (COVID-19) with ambiguous roles of various immune cell compartments. Plasma cells, responsible for antibody production, have a two-pronged response while mounting an immune defence with 1) physiological immune response producing neutralizing antibodies against protein structures of SARS-CoV-2 and 2) potentially deleterious autoantibody generation. Growing evidence hints towards broad activation of plasma cells and the presence of pathologic autoantibodies (abs) that mediate immune perturbation in acute COVID-19 [1]. Recently, a systematic screening for abs confirmed induction of diverse functional abs in SARS-CoV-2 infection, targeting several immunomodulatory proteins, including cytokines/chemokines and their respective G-protein coupled receptors (GPCR) [1]. Abs against GPCR act as agonistic and allosteric receptor modulators and are linked to chronic inflammatory diseases [2] and, as we recently demonstrated, disease severity in acute COVID-19 [3].FootnotesThis manuscript has recently been accepted for publication in the ERJ Open Research. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJOR online. Please open or download the PDF to view this article.Conflict of Interest: Thomas Bahmer reports grants from BMBF: Unrestricted research grant for the German Center for Lung Research (DZL), BMBF: National Pandemic Cohort Network (NAPKON) – Coordinating Study Site for population-based cohort platform; lecture fees from Novartis, AstraZeneca, Chiesi; support for attending ATS Congress from Chiesi; advisory board participation at GlaxoSmithKline, Boehringer Ingelheim, Roche, AstraZeneca; outside the submitted work.Conflict of Interest: Derk Frank reports grants from DFG (467267736), BMBF, DZHK; consulting fees and support for attending meetings from Edwards Lifesciences, Medtronic; lecture honoraria from Edwards Lifesciences, Medtronic, Astra Zeneca, Pfizer, BMS, Novartis, Bayer, Abbott; participation on advisory boards at BMS, Boehringer Ingelheim, Daiichi Sankyo; outside the submitted work.Conflict of Interest: CellTrend is owned by Kai Schulze-Forster. CellTrend is producing ELISA kits for the determination of Antibodies against GPCR.Conflict of Interest: Avi Z. Rosenberg reports grants from NIH (NIDDK, NHLBI); outside the submitted work.Conflict of Interest: Gabriela Riemekasten reports consulting fees from CellTrand GmbH; outside the submitted work.Conflict of Interest: Stefan Schreiber reports consulting fees from Abbvie, Arena, BMS, Biogen, Celltrion, Celgene, IMAB, Gilead, MSD, Mylan, Pfizer, Fresenius, Janssen, Takeda, Theravance, Prevention Bio, Protagonist, Falk; outside the submitted work.Conflict of Interest: All other authors have nothing to disclose. ER -