Evidence map›Paper›PMID 38694513›Full record

ArticleFrontiers in immunology2024

Prevalence of anti-lymphocyte IgM autoantibodies driving complement activation in COVID-19 patients.

Ainhoa Pérez-Díez, Xiangdong Liu, Stephanie Calderon, Ashlynn Bennett, Andrea Lisco, Anela Kellog, Frances Galindo, Matthew J Memoli, Joseph M Rocco, Brian P Epling and 7 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2024. 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
0.8field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
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

17 authors at 4 institutions in 1 country.

Ainhoa Pérez-DíezLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Xiangdong LiuLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Stephanie CalderonLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Ashlynn BennettLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Andrea LiscoLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Anela KellogLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Frances GalindoDivision of Clinical Research, NIAID, NIH, Bethesda, MD, United States.
Matthew J MemoliLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Joseph M RoccoLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Brian P EplingLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Elizabeth LaidlawLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Mike C SnellerLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Maura ManionLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
Glenn W WortmannSection of Infectious Diseases, MedStar Washington Hospital Center, Washington, DC, United States.
Rita PoonDivision of Hospital Medicine, Georgetown University Medical Center, Washington, DC, United States.
Princy KumarDivision of Infectious Diseases and Tropical Medicine, Georgetown University Medical Center, Washington, DC, United States.
Irini SeretiLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, United States.
National Institute of Allergy and Infectious Diseases · USGeorgetown University Medical Center · USMedStar Washington Hospital Center · USNational Institutes of Health Clinical Center · US

Funding

Coronavirus Pathogenesis and Broadly Protective Vaccine DevelopmentZIAAI001268 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MEMOLI, MATTHEW · 2020 to 2025
$4.8M
Pathogenesis of Secondary Hemophagocytic LymphohistiocytosisZIAAI001377 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ROCCO, JOSEPH · 2024 to 2025
$3.0M
Role of lymphopenia and inflammation in COVID-19 pathogenesisZIAAI001308 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SERETI, IRINI · 2020 to 2024
$743k
Identification of immunological predictors of COVID-19 clinical outcomesZIAAI001309 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LISCO, ANDREA · 2020 to 2024
$107k
6 · The paper itself

Abstract

Introduction: COVID-19 patients can develop autoantibodies against a variety of secreted and membrane proteins, including some expressed on lymphocytes. However, it is unclear what proportion of patients might develop anti-lymphocyte antibodies (ALAb) and what functional relevance they might have. Methods: We evaluated the presence and lytic function of ALAb in the sera of a cohort of 85 COVID-19 patients (68 unvaccinated and 17 vaccinated) assigned to mild (N=63), or moderate/severe disease (N=22) groups. Thirty-seven patients were followed-up after recovery. We also analyzed in vivo complement deposition on COVID-19 patients' lymphocytes and examined its correlation with lymphocyte numbers during acute disease. Results: Compared with healthy donors (HD), patients had an increased prevalence of IgM ALAb, which was significantly higher in moderate/severe disease patients and persisted after recovery. Sera from IgM ALAb+ patients exhibited complement-dependent cytotoxicity (CDC) against HD lymphocytes. Complement protein C3b deposition on patients' CD4 T cells was inversely correlated with CD4 T cell numbers. This correlation was stronger in moderate/severe disease patients. Discussion: IgM ALAb and complement activation against lymphocytes may contribute to the acute lymphopenia observed in COVID-19 patients.

Indexed as

AutoantibodiesComplement ActivationCOVID-19Immunoglobulin MSARS-CoV-2AdultAgedCD4-Positive T-LymphocytesComplement C3bFemaleHumansLymphocytesLymphopeniaMaleMiddle AgedPrevalenceAutoantibodiesComplement C3bImmunoglobulin Manti-lymphocyte Abautoantibodiescomplement activationcomplement-dependent cytotoxicitycomplement depositionconvalescent COVID-19COVID-19lymphopenia

Identifiers

PMID38694513
PMCPMC11061367
OpenAlexW4394890122

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.