C1 esterase inhibitor-mediated immunosuppression in COVID-19: Friend or foe?

Clinical Immunology Communications

Kaysie L. Banton¹  David Bar-Or¹  Michael Roshon²  Jason S. Williams²  Melissa A. Hausburg³  Charles W. Mains³ 

[1] Department of Trauma Research, Penrose Hospital, 2222 N Nevada Ave, Colorado Springs, CO 80907, USA;Department of Trauma Research, St. Anthony Hospital, 11600 W 2nd Pl, Lakewood, CO 80228, USA;Department of Trauma Research, Swedish Medical Center, 501 E. Hampden, Englewood, CO 80113, USA;

关键词: COVID-19;    C1-INH;    C1 esterase inhibitor;    Complement;    Inflammation;    FXII;   

DOI  :  

来源: DOAJ

【 摘 要 】

From asymptomatic to severe, SARS-CoV-2, causative agent of COVID-19, elicits varying disease severities. Moreover, understanding innate and adaptive immune responses to SARS-CoV-2 is imperative since variants such as Omicron negatively impact adaptive antibody neutralization. Severe COVID-19 is, in part, associated with aberrant activation of complement and Factor XII (FXIIa), initiator of contact system activation. Paradoxically, a protein that inhibits the three known pathways of complement activation and FXIIa, C1 esterase inhibitor (C1-INH), is increased in COVID-19 patient plasma and is associated with disease severity. Here we review the role of C1-INH in the regulation of innate and adaptive immune responses. Additionally, we contextualize regulation of C1-INH and SERPING1, the gene encoding C1-INH, by other pathogens and SARS viruses and propose that viral proteins bind to C1-INH to inhibit its function in severe COVID-19. Finally, we review the current clinical trials and published results of exogenous C1-INH treatment in COVID-19 patients.

【 授权许可】

Unknown