Risk surveillance and mitigation: autoantibodies as triggers and inhibitors of severe reactions to SARS-CoV-2 infection

Molecular Medicine

Ivo Mueller¹  Aisah Amelia¹  George W. Ashdown¹  Emily M. Eriksson¹  Catherine Chen¹  Anna K. Coussens² 

[1] The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, 3052, Parkville, VIC, Australia;Department of Medical Biology, The University of Melbourne, 3052, Melbourne, VIC, Australia;The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, 3052, Parkville, VIC, Australia;Department of Medical Biology, The University of Melbourne, 3052, Melbourne, VIC, Australia;Department of Pathology, Institute of Infectious Disease and Molecular Medicine, Wellcome Centre for Infectious Diseases Research in Africa, University of Cape, Cape Town, South Africa;

关键词: Autoantibodies;    SARS-CoV-2;    COVID-19;    Autoimmunity;   

DOI  :  10.1186/s10020-021-00422-z

来源: Springer

【 摘 要 】

COVID-19 clinical presentation differs considerably between individuals, ranging from asymptomatic, mild/moderate and severe disease which in some cases are fatal or result in long-term effects. Identifying immune mechanisms behind severe disease development informs screening strategies to predict who are at greater risk of developing life-threatening complications. However, to date clear prognostic indicators of individual risk of severe or long COVID remain elusive. Autoantibodies recognize a range of self-antigens and upon antigen recognition and binding, important processes involved in inflammation, pathogen defence and coagulation are modified. Recent studies report a significantly higher prevalence of autoantibodies that target immunomodulatory proteins including cytokines, chemokines, complement components, and cell surface proteins in COVID-19 patients experiencing severe disease compared to those who experience mild or asymptomatic infections. Here we discuss the diverse impacts of autoantibodies on immune processes and associations with severe COVID-19 disease.

【 授权许可】

CC BY