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