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10.1172/jci.insight.158362

http://scihub22266oqcxt.onion/10.1172/jci.insight.158362
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suck abstract from ncbi


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pmid35349483      JCI+Insight 2022 ; 7 (9): ä
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  • IgM anti-ACE2 autoantibodies in severe COVID-19 activate complement and perturb vascular endothelial function #MMPMID35349483
  • Casciola-Rosen L; Thiemann DR; Andrade F; Trejo-Zambrano MI; Leonard EK; Spangler JB; Skinner NE; Bailey J; Yegnasubramanian S; Wang R; Vaghasia AM; Gupta A; Cox AL; Ray SC; Linville RM; Guo Z; Searson PC; Machamer CE; Desiderio S; Sauer LM; Laeyendecker O; Garibaldi BT; Gao L; Damarla M; Hassoun PM; Hooper JE; Mecoli CA; Christopher-Stine L; Gutierrez-Alamillo L; Yang Q; Hines D; Clarke WA; Rothman RE; Pekosz A; Fenstermacher KZ; Wang Z; Zeger SL; Rosen A
  • JCI Insight 2022[May]; 7 (9): ä PMID35349483show ga
  • BackgroundSome clinical features of severe COVID-19 represent blood vessel damage induced by activation of host immune responses initiated by the coronavirus SARS-CoV-2. We hypothesized autoantibodies against angiotensin-converting enzyme 2 (ACE2), the SARS-CoV-2 receptor expressed on vascular endothelium, are generated during COVID-19 and are of mechanistic importance.MethodsIn an opportunity sample of 118 COVID-19 inpatients, autoantibodies recognizing ACE2 were detected by ELISA. Binding properties of anti-ACE2 IgM were analyzed via biolayer interferometry. Effects of anti-ACE2 IgM on complement activation and endothelial function were demonstrated in a tissue-engineered pulmonary microvessel model.ResultsAnti-ACE2 IgM (not IgG) autoantibodies were associated with severe COVID-19 and found in 18/66 (27.2%) patients with severe disease compared with 2/52 (3.8%) of patients with moderate disease (OR 9.38, 95% CI 2.38-42.0; P = 0.0009). Anti-ACE2 IgM autoantibodies were rare (2/50) in non-COVID-19 ventilated patients with acute respiratory distress syndrome. Unexpectedly, ACE2-reactive IgM autoantibodies in COVID-19 did not undergo class-switching to IgG and had apparent KD values of 5.6-21.7 nM, indicating they are T cell independent. Anti-ACE2 IgMs activated complement and initiated complement-binding and functional changes in endothelial cells in microvessels, suggesting they contribute to the angiocentric pathology of COVID-19.ConclusionWe identify anti-ACE2 IgM as a mechanism-based biomarker strongly associated with severe clinical outcomes in SARS-CoV-2 infection, which has therapeutic implications.FUNDINGBill & Melinda Gates Foundation, Gates Philanthropy Partners, Donald B. and Dorothy L. Stabler Foundation, and Jerome L. Greene Foundation; NIH R01 AR073208, R01 AR069569, Institutional Research and Academic Career Development Award (5K12GM123914-03), National Heart, Lung, and Blood Institute R21HL145216, and Division of Intramural Research, National Institute of Allergy and Infectious Diseases; National Science Foundation Graduate Research Fellowship (DGE1746891).
  • |*Angiotensin-Converting Enzyme 2[MESH]
  • |*COVID-19[MESH]
  • |Autoantibodies[MESH]
  • |Endothelial Cells[MESH]
  • |Humans[MESH]
  • |Immunoglobulin M[MESH]


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