Evidence map›Paper›PMID 32035179›Full record

ArticleClinical immunology (Orlando, Fla.)2020

B cells in rheumatoid arthritis synovial tissues encode focused antibody repertoires that include antibodies that stimulate macrophage TNF-α production.

Serra E Elliott, Sarah Kongpachith, Nithya Lingampalli, Julia Z Adamska, Bryan J Cannon, Lisa K Blum, Michelle S Bloom, Matthew Henkel, Mandy J McGeachy, Larry W Moreland and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Cross-presentation of citrullinated antigens drives cytotoxic CD8bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. B cell tolerance and autoimmunity: Lessons from repertoires.The Journal of experimental medicine · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

11 authors at 3 institutions in 1 country.

Serra E ElliottDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Sarah KongpachithDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Nithya LingampalliDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Julia Z AdamskaDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Bryan J CannonDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Lisa K BlumDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Michelle S BloomDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America.
Matthew HenkelDivision of Rheumatology & Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, United States of America.
Mandy J McGeachyDivision of Rheumatology & Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, United States of America.
Larry W MorelandDivision of Rheumatology & Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, United States of America.
William H RobinsonDivision of Immunology and Rheumatology, Stanford University, Stanford, CA, United States of America; VA Palo Alto Health Care System, Palo Alto, CA, United States of America. Electronic address: w.robinson@stanford.edu.
Stanford University · USUniversity of Pittsburgh · USVA Palo Alto Health Care System · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Prevention Center U01: Early Targets for Antigen-Specific Tolerance Induction in Preclinical Rheumatoid ArthritisU01AI101981 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2012 to 2021
$6.2M
Large-Scale Characterization of Autoantibody Responses in Rheumatoid ArthritisR01AR063676 · NIAMS · STANFORD UNIVERSITY · PI ROBINSON, WILLIAM H · 2013 to 2017
$1.7M
NIAID NIH HHS T32 AI007290NIAID NIH HHS U01 AI101981NIAMS NIH HHS R01 AR063676
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is characterized by the production of anti-citrullinated protein antibodies (ACPAs). To gain insights into the relationship between ACPA-expressing B cells in peripheral blood (PB) and synovial tissue (ST), we sequenced the B cell repertoire in paired PB and ST samples from five individuals with established, ACPA+ RA. Bioinformatics analysis of paired heavy- and light-chain sequences revealed clonally-related family members shared between PB and ST. ST-derived antibody repertoires exhibited reduced diversity and increased normalized clonal family size compared to PB-derived repertoires. Functional characterization showed that seven recombinant antibodies (rAbs) expressed from subject-derived sequences from both compartments bound citrullinated antigens and immune complexes (ICs) formed using one ST-derived rAb stimulated macrophage TNF-α production. Our findings demonstrate B cell trafficking between PB and ST in subjects with RA and ST repertoires include B cells that encode ACPA capable of forming ICs that stimulate cellular responses implicated in RA pathogenesis.

Indexed as

Antibody DiversityAnti-Citrullinated Protein AntibodiesAntigen-Antibody ComplexArthritis, RheumatoidB-LymphocytesComputational BiologyHumansMacrophage ActivationMacrophagesSynovial MembraneTumor Necrosis Factor-alphaAnti-Citrullinated Protein AntibodiesAntigen-Antibody ComplexTNF protein, humanTumor Necrosis Factor-alphaACPAAntibody repertoire sequencingInflammationPeripheral bloodRheumatoid arthritisSynovial tissue

Identifiers

PMID32035179
PMCPMC7327984
OpenAlexW3005462348

What OpenQuestion holds

Textmetadata
LicenceTDM
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.