Evidence map›Paper›PMID 34478165›Full record

ReviewImmunology2021

Crosstalk between B cells and neutrophils in rheumatoid arthritis.

Utsa Karmakar, Sonja Vermeren

Open access · hybridAbstract readReview
In one paragraph

Review in Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Comprehensive Assessment of Neutrophil Function in Autoimmune Diseases.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. NETs: a new target for autoimmune disease.Frontiers in immunology · 2025
    Review
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Utsa KarmakarCentre for Inflammation Research, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh, UK.ORCID 0000-0001-5323-3500
Sonja VermerenCentre for Inflammation Research, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-8460-0884
Centre for Inflammation Research · GB

Funding

Medical Research Council MR/S008020/1Versus Arthritis 21577
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease without known cure that primarily affects synovial joints. RA has a prevalence of approximately 1% of the population worldwide. A vicious circle between two critical immune cell types, B cells and neutrophils, develops and promotes disease. Pathogenic anti-citrullinated protein antibodies (ACPA) directed against a range of citrullinated epitopes are abundant in both plasma and synovial fluid of RA patients. In addition to stimulating numerous cell types, ACPA and other autoantibodies, notably rheumatoid factor, form immune complexes (ICs) that potently activate neutrophils. Attracted to the synovium by abundant chemokines, neutrophils are locally stimulated by ICs. They generate cytokines and release cytotoxic compounds including neutrophil extracellular traps (NETs), strands of decondensed chromatin decorated with citrullinated histones and granule-derived neutrophil proteins, which are particularly abundant in the synovial fluid. In this way, neutrophils generate citrullinated epitopes and release peptidylarginine deiminase (PAD) enzymes capable of citrullinating extracellular proteins in the rheumatic joint, contributing to renewed ACPA generation. This review article focusses on the central function of citrullination, a post-translational modification of arginine residues in RA. The discussion includes ACPA and related autoantibodies, somatic hypermutation-mediated escape from negative selection by autoreactive B cells, promotion of the dominance of citrullinated antigens by genetic and lifestyle susceptibility factors and the vicious circle between ACPA-producing pathogenic B cells and NET-producing neutrophils in RA.

Indexed as

AnimalsArthritis, RheumatoidAutoantigensAutoimmunityBiomarkersB-LymphocytesCell CommunicationDisease SusceptibilityDysbiosisExtracellular TrapsGenetic Predisposition to DiseaseHumansImmunityImmunomodulationNeutrophilsRisk FactorsAutoantigensBiomarkersanti-citrullinated protein antibodiesB cellscitrullinationdysbiosisimmune complexesneutrophil extracellular trapsneutrophilspeptidylarginine deiminaserheumatoid arthritis

Identifiers

PMID34478165
PMCPMC8561113
OpenAlexW3198528619

What OpenQuestion 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 OpenQuestion graph.