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J Clin Invest
. 2021 Oct 28;e154886.
doi: 10.1172/JCI154886. Online ahead of print.
The intersection of COVID-19 and autoimmunity
Jason S Knight 1 , Roberto Caricchio 2 , Jean Laurent Casanova 3 , Alexis J Combes 4 , Betty Diamond 5 , Sharon E Fox 6 , David A Hanauer 7 , Judith A James 8 , Yogendra Kanthi 9 , Virginia Ladd 10 , Puja Mehta 11 , Aaron M Ring 12 , Ignacio Sanz 13 , Carlo Selmi 14 , Russell P Tracy 15 , Paul J Utz 16 , Catriona A Wagner 17 , Julia Y Wang 18 , W Joseph McCune 1
Affiliations
- PMID: 34710063
- DOI: 10.1172/JCI154886
Abstract
Acute coronavirus disease 2019 (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 Disease Association (AARDA) 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.