Evidence map›Paper›PMID 37093875›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2023

Human CCR6+ Th Cells Show Both an Extended Stable Gradient of Th17 Activity and Imprinted Plasticity.

Satya P Singh, Farhat Parween, Nithin Edara, Hongwei H Zhang, Jinguo Chen, Francisco Otaizo-Carrasquero, Debby Cheng, Nicole A Oppenheim, Amy Ransier, Wenjun Zhu and 7 more

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Altered memory CCR6EBioMedicine · 2024
    Article
  5. Frontiers in immunology · 2024
    Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 1 institution in 1 country.

Satya P SinghLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Farhat ParweenLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0001-9535-1679
Nithin EdaraLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0001-6191-1199
Hongwei H ZhangLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Jinguo ChenCenter for Human Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Francisco Otaizo-CarrasqueroResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0001-7518-173X
Debby ChengLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-8360-9780
Nicole A OppenheimLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Amy RansierGenome Analysis Core, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Wenjun ZhuRetinal Neurophysiology Section, National Eye Institute, National Institutes of Health, Bethesda, MD.
Amirhossein ShamsaddiniResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-7830-304X
Paul J GardinaResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Samuel W DarkoHuman Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-9711-8122
Tej Pratap SinghLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-0122-1089
Daniel C DouekHuman Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Timothy G MyersResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-7059-5906
Joshua M FarberLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0003-3224-0378
National Institutes of Health · US

Funding

Infectious Diseases Research Technologies Core - RMLZICAI001052 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$133.3M
Activities Of Chemokines In VivoZIAAI000725 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FARBER, JOSHUA M · 2009 to 2025
$25.5M
The Genome Analysis CoreZICAI005133 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DOUEK, DANIEL CESAR · 2019 to 2025
$16.9M
Intramural NIH HHS ZIA AI000725
6 · The paper itself

Abstract

Th17 cells have been investigated in mice primarily for their contributions to autoimmune diseases. However, the pathways of differentiation of Th17 and related Th cells (type 17 cells) and the structure of the type 17 memory population in humans are not well understood; such understanding is critical for manipulating these cells in vivo. By exploiting differences in levels of surface CCR6, we found that human type 17 memory cells, including individual T cell clonotypes, form an elongated continuum of type 17 character along which cells can be driven by increasing RORγt. This continuum includes cells preserved within the memory pool with potentials that reflect the early preferential activation of multiple over single lineages. The phenotypes and epigenomes of CCR6+ cells are stable across cell divisions under noninflammatory conditions. Nonetheless, activation in polarizing and nonpolarizing conditions can yield additional functionalities, revealing, respectively, both environmentally induced and imprinted mechanisms that contribute differentially across the type 17 continuum to yield the unusual plasticity ascribed to type 17 cells.

Indexed as

Autoimmune DiseasesTh17 CellsCell DifferentiationHumansPhenotypeReceptors, CCR6Th1 CellsCCR6 protein, humanReceptors, CCR6

Identifiers

PMID37093875
PMCPMC10463241
OpenAlexW4366819279

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.