C1 esterase inhibitor-mediated immunosuppression in COVID-19: Friend or foe?
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
Journal
Clinical immunology communications
ISSN: 2772-6134
Titre abrégé: Clin Immunol Commun
Pays: United States
ID NLM: 9918697481206676
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
08
04
2022
revised:
03
05
2022
accepted:
03
05
2022
medline:
28
11
2023
pubmed:
28
11
2023
entrez:
28
11
2023
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 38013973
doi: 10.1016/j.clicom.2022.05.001
pii: S2772-6134(22)00013-0
pmc: PMC9068237
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
83-90Informations de copyright
© 2022 The Authors.
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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