C1 esterase inhibitor-mediated immunosuppression in COVID-19: Friend or foe?
Clin Immunol Commun
; 2: 83-90, 2022 Dec.
Article
em En
| MEDLINE
| ID: mdl-38013973
ABSTRACT
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.
C1 esterase inhibitor; C1 esterase inhibitor, C1-INH; C1-INH; COVID-19; Complement; FXII; Inflammation; Middle East respiratory syndrome coronavirus, MERS-CoV; Mycobacterium tuberculosis, Mtb; Severe acute respiratory syndrome coronavirus, SARS-CoV; acquired C1-INH deficiency, AEE; activated plasma kallikrein, PKa; antibody-mediated rejection, AMR; bradykinin, BK; contact system, CS; coronavirus disease 2019, COVID-19; exogenous C1-INH, exC1-INH; hereditary angioedema, HAE; high-molecular-weight kininogen, HK; human immunodeficiency virus, HIV; interferon, IFN; interleukin, IL; ischemia/reperfusion injury, IRI; mannose-binding lectin, MBL; prekallikrein, PK; recombinant C1-INH, rhC1-INH; serine protease inhibitor, serpin; tuberculosis, TB
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1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article