Evidence map›Paper›PMID 38013973›Full record

ReviewClinical immunology communications2022

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

Melissa A Hausburg, Jason S Williams, Kaysie L Banton, Charles W Mains, Michael Roshon, David Bar-Or

Open access · goldAbstract readReview
In one paragraph

Review in Clinical immunology communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Trial
  2. Article
  3. Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Melissa A HausburgDepartment of Trauma Research, Swedish Medical Center, 501 E. Hampden, Englewood, CO 80113, USA.
Jason S WilliamsDepartment of Trauma Research, Swedish Medical Center, 501 E. Hampden, Englewood, CO 80113, USA.
Kaysie L BantonDepartment of Trauma Research, Swedish Medical Center, 501 E. Hampden, Englewood, CO 80113, USA.
Charles W MainsCentura Health Trauma Systems, Centura Health, 9100 E Mineral Circle, Centennial, CO 80112, USA.
Michael RoshonCentura Health Trauma Systems, Centura Health, 9100 E Mineral Circle, Centennial, CO 80112, USA.
David Bar-OrDepartment of Trauma Research, Swedish Medical Center, 501 E. Hampden, Englewood, CO 80113, USA.
Penrose Hospital · USRocky Vista University · USSwedish Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

acquired C1-INH deficiency, AEEactivated plasma kallikrein, PKaantibody-mediated rejection, AMRbradykinin, BKC1 esterase inhibitorC1 esterase inhibitor, C1-INHC1-INHComplementcontact system, CScoronavirus disease 2019, COVID-19COVID-19exogenous C1-INH, exC1-INHFXIIhereditary angioedema, HAEhigh-molecular-weight kininogen, HKhuman immunodeficiency virus, HIVInflammationinterferon, IFNinterleukin, ILischemia/reperfusion injury, IRImannose-binding lectin, MBLMiddle East respiratory syndrome coronavirus, MERS-CoVMycobacterium tuberculosis, Mtbprekallikrein, PKrecombinant C1-INH, rhC1-INHserine protease inhibitor, serpinSevere acute respiratory syndrome coronavirus, SARS-CoVtuberculosis, TB

Identifiers

PMID38013973
PMCPMC9068237
OpenAlexW4229007313

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.