Evidence map›Paper›PMID 23045607›Full record

ArticleThe Journal of experimental medicine2012

B and T cells collaborate in antiviral responses via IL-6, IL-21, and transcriptional activator and coactivator, Oct2 and OBF-1.

Alex Karnowski, Stephane Chevrier, Gabrielle T Belz, Adele Mount, Dianne Emslie, Kathy D'Costa, David M Tarlinton, Axel Kallies, Lynn M Corcoran

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03414086 (Predictor of Clinical Response to Acthar in Myositis), which is not on this map. Cited by 133 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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.

NCT03414086 completednot on this mapstarted 2017, after this paper: background citation

Predictor of Clinical Response to Acthar in Myositis: Phase II of Acthar Clinical Trial

TypeobservationalSponsorUniversity of PittsburghRan2017 to 2022Enrolled20ConditionsMyositis, Dermatomyositis, PolymyositisArmsHealthy Control, Myositis in Remission
3 · Its place in the literature

Who cites it

133 citing papers in PubMed, 1 synthesis or guideline pooled it, 195 citations in OpenAlex.

  1. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Journal of fungi (Basel, Switzerland) · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. POU2F2Scientific reports · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. The Complex Dysregulations of CD4 T Cell Subtypes in HIV Infection.International journal of molecular sciences · 2024
    Review
  18. Review
  19. Article
  20. Article

73 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Alex KarnowskiMolecular Immunology Division and 2 Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia.
Stephane Chevrier
Gabrielle T Belz
Adele Mount
Dianne Emslie
Kathy D'Costa
David M Tarlinton
Axel Kallies
Lynn M Corcoran
Center of Molecular Immunology (Cuba) · CUUniversity of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

Medical Research Council
6 · The paper itself

Abstract

A strong humoral response to infection requires the collaboration of several hematopoietic cell types that communicate via antigen presentation, surface coreceptors and their ligands, and secreted factors. The proinflammatory cytokine IL-6 has been shown to promote the differentiation of activated CD4(+) T cells into T follicular helper cells (T(FH) cells) during an immune response. T(FH) cells collaborate with B cells in the formation of germinal centers (GCs) during T cell-dependent antibody responses, in part through secretion of critical cytokines such as IL-21. In this study, we demonstrate that loss of either IL-6 or IL-21 has marginal effects on the generation of T(FH) cells and on the formation of GCs during the response to acute viral infection. However, mice lacking both IL-6 and IL-21 were unable to generate a robust T(FH) cell-dependent immune response. We found that IL-6 production in follicular B cells in the draining lymph node was an important early event during the antiviral response and that B cell-derived IL-6 was necessary and sufficient to induce IL-21 from CD4(+) T cells in vitro and to support T(FH) cell development in vivo. Finally, the transcriptional activator Oct2 and its cofactor OBF-1 were identified as regulators of Il6 expression in B cells.

Indexed as

AnimalsAntibodies, ViralBlotting, WesternB-LymphocytesFlow CytometryGene Expression RegulationGerminal CenterHost-Pathogen InteractionsInfluenza A Virus, H3N2 SubtypeInterleukin-21Interleukin-6InterleukinsMiceMice, Inbred C57BLMice, KnockoutOctamer Transcription Factor-2Antibodies, ViralInterleukin-21Interleukin-6InterleukinsOctamer Transcription Factor-2Pou2af1 protein, mousePou2f2 protein, mouseTrans-Activators

Identifiers

PMID23045607
PMCPMC3478936
OpenAlexW2166079594

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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.