Evidence map›Paper›PMID 35781671›Full record

ReviewImmunological reviews2022

Heterogeneity in IgG-CD16 signaling in infectious disease outcomes.

Joseph C Gonzalez, Saborni Chakraborty, Natalie K Thulin, Taia T Wang

Open access · hybridAbstract readReview
In one paragraph

Review in Immunological reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Immunological Disorders: Gradations and the Current Approach in Laboratory Diagnostics.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Linking Effector Function to Antitumor Monoclonal Antibody Efficacy.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Immunity to SARS-CoV-2 infection.Immunological reviews · 2022
    Article
  17. 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

4 authors at 2 institutions in 1 country.

Joseph C GonzalezDepartment of Medicine, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0002-3282-0041
Saborni ChakrabortyDepartment of Medicine, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0003-0502-3757
Natalie K ThulinDepartment of Immunology, University of Washington, Seattle, Washington, USA.ORCID 0000-0002-7721-3747
Taia T WangDepartment of Medicine, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0002-3894-685X
Stanford University · USUniversity of Washington · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Understanding B cell memory in response to diverse virus infectionsU19AI111825 · NIAID · ROCKEFELLER UNIVERSITY · PI RAVETCH, JEFFREY VICTOR · 2014 to 2023
$26.0M
Regulation of the IgG Fc domain repertoireR01AI139119 · NIAID · STANFORD UNIVERSITY · PI WANG, TAIA · 2019 to 2023
$2.8M
NIAID NIH HHS R01 AI139119NIAID NIH HHS T32 AI007290NIAID NIH HHS U19 AI111825
6 · The paper itself

Abstract

In this review, we discuss how IgG antibodies can modulate inflammatory signaling during viral infections with a focus on CD16a-mediated functions. We describe the structural heterogeneity of IgG antibody ligands, including subclass and glycosylation that impact binding by and downstream activity of CD16a, as well as the heterogeneity of CD16a itself, including allele and expression density. While inflammation is a mechanism required for immune homeostasis and resolution of acute infections, we focus here on two infectious diseases that are driven by pathogenic inflammatory responses during infection. Specifically, we review and discuss the evolving body of literature showing that afucosylated IgG immune complex signaling through CD16a contributes to the overwhelming inflammatory response that is central to the pathogenesis of severe forms of dengue disease and coronavirus disease 2019 (COVID-19).

Indexed as

Communicable DiseasesCOVID-19HumansImmunoglobulin GPolysaccharidesReceptors, IgGImmunoglobulin GPolysaccharidesReceptors, IgGCOVID-19dengue diseaseeffector functionsFc afucosylationIgG1 antibodies

Identifiers

PMID35781671
PMCPMC9539944
OpenAlexW4283797588

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.