Evidence map›Paper›PMID 26408661›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

PLZF Controls the Development of Fetal-Derived IL-17+Vγ6+ γδ T Cells.

Ying Lu, Xin Cao, Xianyu Zhang, Damian Kovalovsky

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

47 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Development of αβ and γδ T Cells in the Thymus and Methods of Analysis.International journal of molecular sciences · 2025
    Review
  3. HEB collaborates with TCR signaling to upregulatebioRxiv : the preprint server for biology · 2025
    Article
  4. Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025
    Review
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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 1 institution in 1 country.

Ying LuExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Xin CaoExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Xianyu ZhangExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Damian KovalovskyExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 kovalovskyd@mail.nih.gov.
National Institutes of Health · US

Funding

Zbtb family members in lymphocyte differentiation and functionZIABC011429 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KOVALOVSKY, DAMIAN · 2012 to 2017
$3.4M
Intramural NIH HHS ZIA BC011429PHS HHS 1ZIABC011429
6 · The paper itself

Abstract

Expression of promyelocytic leukemia zinc finger (PLZF) protein directs the effector differentiation of invariant NKT (iNKT) cells and IL-4(+) γδ NKT cells. In this study, we show that PLZF is also required for the development and function of IL-17(+) γδ T cells. We observed that PLZF is expressed in fetal-derived invariant Vγ5(+) and Vγ6(+) γδ T cells, which secrete IFN-γ and IL-17, respectively. PLZF deficiency specifically affected the effector differentiation of Vγ6(+) cells, leading to reduced numbers of mature CD27(-)CD44(+) phenotype capable of secreting IL-17. Although PLZF was not required for Vγ5(+) γδ T cells to develop, when these cells were reprogrammed into IL-17-secreting cells in Skint-1 mutant mice, they required PLZF for their effector maturation, similarly to Vγ6(+) γδ T cells. The impaired effector differentiation of PLZF-deficient Vγ6(+) γδ T cells was not due to increased apoptosis and it was related to reduced proliferation of immature CD27(+)CD44(-) Vγ6(+) γδ T cells, which was required for their differentiation into mature CD27(-)CD44(+) IL-17-secreting cells. Thus, the present study identifies that PLZF function is not restricted to NKT or IL-4(+) T cells, but it also controls the development of IL-17(+) γδ T cells.

Indexed as

AnimalsAnimals, NewbornCell DifferentiationCell LineageFetusFlow CytometryGene Expression Regulation, DevelopmentalInterleukin-17Kruppel-Like Transcription FactorsMice, Inbred C57BLMice, KnockoutMice, TransgenicPromyelocytic Leukemia Zinc Finger ProteinProto-Oncogene Proteins c-bcl-2Receptors, Antigen, T-Cell, gamma-deltaReverse Transcriptase Polymerase Chain ReactionIl17a protein, mouseInterleukin-17Kruppel-Like Transcription FactorsPromyelocytic Leukemia Zinc Finger ProteinProto-Oncogene Proteins c-bcl-2Receptors, Antigen, T-Cell, gamma-deltaZbtb16 protein, mouse

Identifiers

PMID26408661
PMCPMC4610873
OpenAlexW2218271266

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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.