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Publications

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Review Ppublish 112 citations

PubMed: 34710063 DOI: 10.1172/JCI154886

The intersection of COVID-19 and autoimmunity.

J Clin Invest 131(24)

Authors: Jason S Knight, Roberto Caricchio, Jean-Laurent Casanova, Alexis J Combes, Betty Diamond, Sharon E Fox, David A Hanauer, Judith A James, Yogendra Kanthi, Virginia Ladd, Puja Mehta, Aaron M Ring, Ignacio Sanz, Carlo Selmi, Russell P Tracy, Paul J Utz, Catriona A Wagner, Julia Y Wang, William J McCune

Affiliations

  • Division of Rheumatology, University of Michigan, Ann Arbor, Michigan, USA.
  • Section of Rheumatology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA.
  • St. Giles Laboratory of Human Genetics of Infectious Diseases, The Rockefeller University, New York, New York, USA.
  • Howard Hughes Medical Institute, New York, New York, USA.
  • Laboratory of Human Genetics of Infectious Diseases, INSERM, Necker Hospital for Sick Children, Paris, France.
  • Imagine Institute, University of Paris, Paris, France.
  • Department of Pathology, ImmunoX Initiative, UCSF Immunoprofiler Initiative, UCSF CoLabs, UCSF, San Francisco, California, USA.
  • Center for Autoimmune and Musculoskeletal Diseases, Northwell Health's Feinstein Institute for Medical Research, New York, New York, USA.
  • Pathology and Laboratory Medicine Service, Southeast Louisiana Veterans Healthcare System, New Orleans, Louisiana, USA.
  • Department of Pathology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
  • Department of Pediatrics and School of Information, University of Michigan, Ann Arbor, Michigan, USA.
  • Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
  • National Heart, Lung, and Blood Institute Division of Intramural Research, Bethesda, Maryland, USA.
  • American Autoimmune Related Diseases Association Inc. Eastpointe, Michigan, USA.
  • Centre for Inflammation and Tissue Repair, University College London, London, United Kingdom.
  • Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA.
  • Division of Rheumatology, Emory University, Atlanta, Georgia, USA.
  • Rheumatology and Clinical Immunology, Humanitas Research Hospital-Scientific Institute for Research, Hospitalization and Healthcare, Rozzano, Milan, Italy.
  • Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy.
  • Department of Pathology and Laboratory Medicine and Department of Biochemistry, University of Vermont Larner College of Medicine, Burlington, Vermont, USA.
  • Division of Immunology, Department of Medicine, Stanford University, Stanford, California, USA.
  • Curandis, New York, New York, USA.

Abstract

Acute COVID-19, caused by SARS-CoV-2, is characterized by diverse clinical presentations, ranging from asymptomatic infection to fatal respiratory failure, and often associated with varied longer-term sequelae. Over the past 18 months, it has become apparent that inappropriate immune responses contribute to the pathogenesis of severe COVID-19. Researchers working at the intersection of COVID-19 and autoimmunity recently gathered at an American Autoimmune Related Diseases Association Noel R. Rose Colloquium to address the current state of knowledge regarding two important questions: Does established autoimmunity predispose to severe COVID-19? And, at the same time, can SARS-CoV-2 infection trigger de novo autoimmunity? Indeed, work to date has demonstrated that 10% to 15% of patients with critical COVID-19 pneumonia exhibit autoantibodies against type I interferons, suggesting that preexisting autoimmunity underlies severe disease in some patients. Other studies have identified functional autoantibodies following infection with SARS-CoV-2, such as those that promote thrombosis or antagonize cytokine signaling. These autoantibodies may arise from a predominantly extrafollicular B cell response that is more prone to generating autoantibody-secreting B cells. This Review highlights the current understanding, evolving concepts, and unanswered questions provided by this unique opportunity to determine mechanisms by which a viral infection can be exacerbated by, and even trigger, autoimmunity. The potential role of autoimmunity in post-acute sequelae of COVID-19 is also discussed.

MeSH

Infections, Work, Autoantibodies, Autoimmunity, Cells, B-Lymphocytes, Covid-19, Sars-Cov-2

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