Evidence map›Paper›PMID 24080164›Full record

ArticleCytokine2014

In vitro generated Th17 cells support the expansion and phenotypic stability of CD4(+)Foxp3(+) regulatory T cells in vivo.

Qiong Zhou, Ya Hu, O M Zack Howard, Joost J Oppenheim, Xin Chen

Abstract read
In one paragraph

Article in Cytokine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Decoding TNF receptor superfamily control of CD4Cell communication and signaling : CCS · 2026
    Review
  3. Article
  4. Eutopic Endometrium Immune Changes Involved in Development and Progression of Endometriosis: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. TNF-TNFR2 Signal Plays a Decisive Role in the Activation of CD4Advances in experimental medicine and biology · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Th17 Responses to Collagen Type V, kα1-Tubulin, and Vimentin Are Present Early in Human Development and Persist Throughout Life.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017
    Article
  14. Article
  15. Article
  16. Review
  17. Th17 cells and Tregs: unlikely allies.Journal of leukocyte biology · 2014
    Review
  18. 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

5 authors at 2 institutions in 1 country.

Qiong ZhouLaboratory of Molecular Immunoregulation, Cancer Inflammation Program, Center for Cancer Research, NCI, Frederick, MD 21702, United States.
Ya Hu
O M Zack Howard
Joost J Oppenheim
Xin Chen
Center for Cancer Research · USScience Applications International Corporation (United States) · US

Funding

Role of T regulatory suppression in autoimmunity and cancerZIABC010707 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OPPENHEIM, JOOST J · 2009 to 2022
$4.9M
CCR NIH HHS HHSN261200800001CIntramural NIH HHS Z99 CA999999NCI NIH HHS HHSN261200800001ENCI NIH HHS Y99 CA999999
6 · The paper itself

Abstract

CD4(+) T cells stimulate immune responses through distinct patterns of cytokine produced by Th1, Th2 or Th17 cells, or inhibit immune responses through Foxp3-expressing regulatory T cells (Tregs). Paradoxically, effector T cells were recently shown to activate Tregs, however, it remains unclear which Th subset is responsible for this effect. In this study, we found that Th17 cells expressed the highest levels of TNF among in vitro generated Th subsets, and most potently promoted expansion and stabilized Foxp3 expression by Tregs when co-transferred into Rag1(-/-) mice. Both TNF and IL-2 produced by Th17 cells contributed to this effect. The stimulatory effect of Th17 cells on Tregs was largely abolished when co-transferred with TNFR2-deficient Tregs. Furthermore, Tregs deficient in TNFR2 also supported a much lower production of IL-17A and TNF expression by co-transferred Th17 cells. Thus, our data indicate that the TNF-TNFR2 pathway plays a crucial role in the reciprocal stimulatory effect of Th17 cells and Tregs. This bidirectional interaction should be taken into account when designing therapy targeting Th17 cells, Tregs, TNF and TNFR2.

Indexed as

Adoptive TransferAnimalsCD4 AntigensCytokinesForkhead Transcription FactorsInterleukin-17Interleukin-2Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutReceptors, Tumor Necrosis Factor, Type IITh17 CellsTh1 CellsTh2 CellsT-Lymphocytes, RegulatoryCD4 AntigensCytokinesForkhead Transcription FactorsFoxp3 protein, mouseIl17a protein, mouseInterleukin-17Interleukin-2Receptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaeffector T cellsforkhead box P3FoxP3IL-2KIknock inknock outKOnaïve CD4 cellsnCD4Regulatory T cellregulatory T cellsTeffsTh17TNFTNFR2TNFR2-FcTNFR2 Fc fusion proteinTregstumor necrosis factor receptor type II

Identifiers

PMID24080164
PMCPMC3842389
OpenAlexW2006896453

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.