Evidence map›Paper›PMID 26468051›Full record

ReviewCellular and molecular life sciences : CMLS2016

The common γ-chain cytokine receptor: tricks-and-treats for T cells.

Adam T Waickman, Joo-Young Park, Jung-Hyun Park

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

53 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
  2. Regulatory T cells: From Foxp3 to tolerance-inducing therapies.The Journal of investigative dermatology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. CCR2Cellular & molecular immunology · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Pathways and mechanisms of CD4Trends in immunology · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

Adam T WaickmanExperimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bldg. 10, Room 5B17, 10 Center Dr, Bethesda, MD, 20892, USA.
Joo-Young ParkExperimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bldg. 10, Room 5B17, 10 Center Dr, Bethesda, MD, 20892, USA.
Jung-Hyun ParkExperimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bldg. 10, Room 5B17, 10 Center Dr, Bethesda, MD, 20892, USA. parkhy@mail.nih.gov.
National Institutes of Health · US

Funding

Post-Transcriptional Regulation of Interleukin-7 Receptor ExpressionZIABC011214 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PARK, JUNG-HYUN · 2009 to 2025
$15.9M
Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Originally identified as the third subunit of the high-affinity IL-2 receptor complex, the common γ-chain (γc) also acts as a non-redundant receptor subunit for a series of other cytokines, collectively known as γc family cytokines. γc plays essential roles in T cell development and differentiation, so that understanding the molecular basis of its signaling and regulation is a critical issue in T cell immunology. Unlike most other cytokine receptors, γc is thought to be constitutively expressed and limited in its function to the assembly of high-affinity cytokine receptors. Surprisingly, recent studies reported a series of findings that unseat γc as a simple housekeeping gene, and unveiled γc as a new regulatory molecule in T cell activation and differentiation. Cytokine-independent binding of γc to other cytokine receptor subunits suggested a pre-association model of γc with proprietary cytokine receptors. Also, identification of a γc splice isoform revealed expression of soluble γc proteins (sγc). sγc directly interacted with surface IL-2Rβ to suppress IL-2 signaling and to promote pro-inflammatory Th17 cell differentiation. As a result, endogenously produced sγc exacerbated autoimmune inflammatory disease, while the removal of endogenous sγc significantly ameliorated disease outcome. These data provide new insights into the role of both membrane and soluble γc in cytokine signaling, and open new venues to interfere and modulate γc signaling during immune activation. These unexpected discoveries further underscore the perspective that γc biology remains largely uncharted territory that invites further exploration.

Indexed as

Alternative SplicingAnimalsCytokinesHumansInflammationInterleukin Receptor Common gamma SubunitJanus Kinase 3Lymphocyte ActivationProtein IsoformsReceptors, CytokineSignal TransductionTh17 CellsT-LymphocytesCytokinesInterleukin Receptor Common gamma SubunitJanus Kinase 3Protein IsoformsReceptors, CytokineAlternative splicingHomeostasisJAK3SignalingSurvival

Identifiers

PMID26468051
PMCPMC6315299
OpenAlexW1960396018

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.