Evidence map›Paper›PMID 23112125›Full record

ArticleEuropean journal of immunology2013

Lymphotoxin α1β2 expression on B cells is required for follicular dendritic cell activation during the germinal center response.

Riley C Myers, R Glenn King, Robert H Carter, Louis B Justement

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2013. 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
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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Lymphotoxin beta receptorInfection and immunity · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Regulation of the Germinal Center Response.Frontiers in immunology · 2018
    Review
  11. Article
  12. ICOS Co-Stimulation: Friend or Foe?Frontiers in immunology · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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

4 authors at 2 institutions in 1 country.

Riley C MyersDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
R Glenn King
Robert H Carter
Louis B Justement
University of Alabama at Birmingham · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
CD19 TYROSINE MEDIATED SIGNAL TRANSDUCTION IN VIVOR01AI042265 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JUSTEMENT, LOUIS B · 1998 to 2012
$4.0M
NIAID NIH HHS AI042265-13NIAID NIH HHS R01 AI042265NIAID NIH HHS T32 AI007051NIAMS NIH HHS P30 AR048311
6 · The paper itself

Abstract

CD19-deficient mice were used as a model to study follicular dendritic cell (FDC) activation because these mice have normal numbers of FDC-containing primary follicles, but lack the ability to activate FDCs or form GCs. It was hypothesized that CD19 expression is necessary for B-cell activation and upregulation of membrane lymphotoxin (mLT) expression, which promotes FDC activation. Using VCAM-1 and FcγRII/III as FDC activation markers, it was determined that the adoptive transfer of CD19(+) wild-type B cells into CD19-deficient hosts rescued GC formation and FDC activation, demonstrating that CD19 expression on B cells is required for FDC activation. In contrast, CD19(+) donor B cells lacking mLT were unable to induce VCAM-1 expression on FDCs, furthermore FcγRII/III upregulation was impaired in FDCs stimulated with mLT-deficient B cells. VCAM-1 expression on FDCs, but not FcγRII/III, was rescued when CD19-deficient B cells expressing transgenic mLT were cotransferred into recipient mice with CD19(+) , mLT-deficient B cells, suggesting that FDC activation requires the CD19-dependent upregulation of mLT on activated B cells. Collectively, these data demonstrate that activated B cells are responsible for the initiation of FDC activation resulting in a microenvironment supportive of GC development and maintenance.

Indexed as

AnimalsAntigens, CD19B-LymphocytesDendritic Cells, FollicularGerminal CenterLymphocyte ActivationLymphotoxin alpha1, beta2 HeterotrimerMiceMice, Inbred C57BLReceptors, IgGUp-RegulationVascular Cell Adhesion Molecule-1Antigens, CD19Lymphotoxin alpha1, beta2 HeterotrimerReceptors, IgGVascular Cell Adhesion Molecule-1

Identifiers

PMID23112125
PMCPMC3753018
OpenAlexW1532609728

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.