Evidence map›Paper›PMID 27121060›Full record

ArticleOncotarget2016

Collaboration between tumor-specific CD4+ T cells and B cells in anti-cancer immunity.

Thomas V Guy, Alexandra M Terry, Holly A Bolton, David G Hancock, Erhua Zhu, Robert Brink, Helen M McGuire, Elena Shklovskaya, Barbara Fazekas de St. Groth

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. TLR3 Activation of Intratumoral CD103Frontiers in immunology · 2019
    Article
  9. 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

9 authors at 3 institutions in 1 country.

Thomas V GuyT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Alexandra M TerryT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Holly A BoltonT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
David G HancockT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Erhua ZhuT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Robert BrinkB Cell Laboratory, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
Helen M McGuireT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Elena ShklovskayaT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Barbara Fazekas de St. GrothT Cell Biology Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, The University of Sydney, Sydney, NSW, Australia.
Centenary Institute · AUUniversity of Sydney · AUGarvan Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of B cells and antibodies in anti-tumor immunity is controversial, with both positive and negative effects reported in animal models and clinical studies. We developed a murine B16.F10 melanoma model to study the effects of collaboration between tumor-specific CD4+ T cells and B cells on tumor control. By incorporating T cell receptor transgenic T cells and B cell receptor isotype switching B cells, we were able to track the responses of tumor-reactive T and B cells and the development of anti-tumor antibodies in vivo. In the presence of tumor-specific B cells, the number of tumor-reactive CD4+ T cells was reduced in lymphoid tissues and the tumor itself, and this correlated with poor tumor control. B cells had little effect on the Th1 bias of the CD4+ T cell response, and the number of induced FoxP3+ regulatory cells (iTregs) generated from within the original naive CD4+ T cell inoculum was unrelated to the degree of B cell expansion. In response to CD4+ T cell help, B cells produced a range of isotype-switched anti-tumor antibodies, principally IgG1, IgG2a/c and IgG2b. In the absence of CD4+ T cells, B cells responded to agonistic anti-CD40 administration by switching to production of IgG2a/c and, to a lesser extent, IgG1, IgG3, IgA and IgE, which reduced the number of lung metastases after i.v. tumor inoculation but had no effect on the growth of subcutaneous tumors.

Indexed as

AnimalsAntibody FormationB-LymphocytesCD4-Positive T-LymphocytesCell DifferentiationCell Line, TumorCytokinesImmunoglobulin Class SwitchingKaplan-Meier EstimateLymphocyte ActivationMelanoma, ExperimentalMice, Inbred C57BLMice, KnockoutMice, TransgenicTumor BurdenCytokinesantibodyB cellCD4 T cellImmune responseImmunityImmunology and Microbiology Sectionmelanoma

Identifiers

PMID27121060
PMCPMC5058675
OpenAlexW2338368944

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.