Evidence map›Paper›PMID 33083808›Full record

ArticlemedRxiv : the preprint server for health sciences2020

IgM autoantibodies recognizing ACE2 are associated with severe COVID-19.

Livia Casciola-Rosen, David R Thiemann, Felipe Andrade, Maria Isabel Trejo Zambrano, Jody E Hooper, Elissa K Leonard, Jamie B Spangler, Andrea L Cox, Carolyn E Machamer, Lauren Sauer and 15 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 3 institutions in 1 country.

Livia Casciola-RosenDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
David R ThiemannDepartment of Medicine, Divisioin of Cardiology, Jhohns Hopkins University School of Medicine, Baltimore, Maryland.
Felipe AndradeDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Maria Isabel Trejo ZambranoDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Jody E HooperDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Elissa K LeonardDepartment of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Jamie B SpanglerDepartment of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Andrea L CoxDepartment of Medicine, Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Carolyn E MachamerDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Lauren SauerJohns Hopkins Hospital, Adult Emergency Department, Baltimore, Maryland.
Oliver LaeyendeckerDivision of Intramural Medicine, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Baltimore, Maryland.
Brian T GaribaldiJohns Hopkins Biocontainment Unit, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Stuart C RayDepartment of Medicine, Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Christopher A MecoliDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Lisa Christopher-StineDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Laura Gutierrez-AlamilloDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Qingyuan YangDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
David HinesDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
William A ClarkeDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Richard RothmanJohns Hopkins Hospital, Adult Emergency Department, Baltimore, Maryland.
Andrew PekoszDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland.
Katherine J FenstermacherDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland.
Zitong WangDepartment of Bioistatistics, Bloomberg School of Public Health, Baltimore, Maryland.
Scott L ZegerDepartment of Bioistatistics, Bloomberg School of Public Health, Baltimore, Maryland.
Antony RosenDepartment of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Johns Hopkins University · USJohns Hopkins Hospital · USNational Institutes of Health · US

Funding

Sample Processing and Immunoassay Research CoreP30AR070254 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI CLIFTON O BINGHAM, Antony Rosen · 2016 to 2026
$8.9M
Autoantibodies Define Scleroderma Subgroups with Distinct Relationships to CancerR01AR073208 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI LIVIA A CASCIOLA-ROSEN, Ami Aalok Shah · 2018 to 2026
$5.2M
ASPIRE - A Joint Johns Hopkins, Morgan State and Coppin State IRACDA ProgramK12GM123914 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI BROWN, LISA D., SARMA, SRIDEVI V. · 2018 to 2022
$2.5M
The role of complement citrullination in RA pathogenesisR01AR069569 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ANDRADE, FELIPE · 2016 to 2020
$1.8M
Optimizing the Approach to Identify Cancer-Associated MyositisK23AR075898 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI MECOLI, CHRISTOPHER · 2019 to 2023
$773k
NIAID NIH HHS HHSN272201400007CNIAMS NIH HHS K23 AR075898NIAMS NIH HHS P30 AR070254NIAMS NIH HHS R01 AR069569NIAMS NIH HHS R01 AR073208NIGMS NIH HHS K12 GM123914
6 · The paper itself

Abstract

SARS-CoV-2 infection induces severe disease in a subpopulation of patients, but the underlying mechanisms remain unclear. We demonstrate robust IgM autoantibodies that recognize angiotensin converting enzyme-2 (ACE2) in 18/66 (27%) patients with severe COVID-19, which are rare (2/52; 3.8%) in hospitalized patients who are not ventilated. The antibodies do not undergo class-switching to IgG, suggesting a T-independent antibody response. Purified IgM from anti-ACE2 patients activates complement. Pathological analysis of lung obtained at autopsy shows endothelial cell staining for IgM in blood vessels in some patients. We propose that vascular endothelial ACE2 expression focuses the pathogenic effects of these autoantibodies on blood vessels, and contributes to the angiocentric pathology observed in some severe COVID-19 patients. These findings may have predictive and therapeutic implications.

Identifiers

PMID33083808
PMCPMC7574257
OpenAlexW3093196145

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.