The intersection of COVID-19 and autoimmunity

• Type of Material: Article
• Authors: Jason S Knight, University of Michigan; Roberto Caricchio, Temple University; Jean-Laurent Casanova, Rockefeller University; Alexis J Combes, UCSF Immunoprofiler Initiative; Betty Diamond, Northwell Healths Feinstein Inst Med Res; Sharon E Fox, Southeast Louisiana Vet Healthcare Syst; David A Hanauer, University of Michigan; Judith A James, Oklahoma Medical Research Foundation; Yogendra Kanthi, National Heart, Lung, and Blood Institute Division of Intramural Research, Bethesda; Virginia Ladd, Amer Autoimmune Related Dis Assoc Inc; Puja Mehta, University College London; Aaron M Ring, Yale School of Medicine; Ignacio Sanz, Emory University; Carlo Selmi, Humanitas Res Hosp Sci Inst Res; Russell P Tracy, University of Vermont; Paul J Utz, Stanford University; Catriona A Wagner, Amer Autoimmune Related Dis Assoc Inc; Julia Y Wang, Curandis; William J McCune, University of Michigan
• Language: English
• Date: 2021-12-15
• Publisher: AMER SOC CLINICAL INVESTIGATION INC
• Publication Version: Final Published Version
• Copyright Statement: © 2021 American Society for Clinical Investigation
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1172/JCI154886
• Title of Journal or Parent Work: JOURNAL OF CLINICAL INVESTIGATION
• Volume: 131
• Issue: 24
• Keywords: Medicine, Research & Experimental; DENDRITIC CELLS; AUTOANTIBODIES; COLONY-STIMULATING FACTOR; Research & Experimental Medicine; Life Sciences & Biomedicine; Science & Technology; INTERFERON-ALPHA; HYPERINFLAMMATION; ANTIBODIES; DERMATAN SULFATE; SYSTEMIC-LUPUS-ERYTHEMATOSUS; NEUTROPHIL EXTRACELLULAR TRAPS; BLOCKADE
• Research Categories: Health Sciences, Pathology

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.