Evidence map›Paper›PMID 36268015›Full record

ReviewFrontiers in immunology2022

Neglected, yet significant role of FOXP1 in T-cell quiescence, differentiation and exhaustion.

Yaroslav Kaminskiy, Varvara Kuznetsova, Anna Kudriaeva, Ekaterina Zmievskaya, Emil Bulatov

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  5. Engineered Foxp1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  13. Review
  14. Role of myofiber-specific FoxP1 in pancreatic cancer-induced muscle wasting.American journal of physiology. Cell physiology · 2025
    Article
  15. 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

5 authors at 4 institutions in 2 countries.

Yaroslav KaminskiyDepartment of Oncology and Pathology, Karolinska Institutet, SciLifeLab, Solna, Sweden.
Varvara KuznetsovaLaboratory of Transplantation Immunology, National Research Centre for Hematology, Moscow, Russia.
Anna KudriaevaShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia.
Ekaterina ZmievskayaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Emil BulatovShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia.
Kazan Federal University · RUFederal State Institution Hematology Research Center · RUInstitute of Bioorganic Chemistry · RUScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FOXP1 is ubiquitously expressed in the human body and is implicated in both physiological and pathological processes including cancer. However, despite its importance the role of FOXP1 in T-cells has not been extensively studied. Although relatively few phenotypic and mechanistic details are available, FOXP1 role in T-cell quiescence and differentiation of CD4+ subsets has recently been established. FOXP1 prevents spontaneous T-cell activation, preserves memory potential, and regulates the development of follicular helper and regulatory T-cells. Moreover, there is growing evidence that FOXP1 also regulates T-cell exhaustion. Altogether this makes FOXP1 a crucial and highly undervalued regulator of T-cell homeostasis. In this review, we discuss the biology of FOXP1 with a focus on discoveries made in T-cells in recent years.

Indexed as

Forkhead Transcription FactorsRepressor ProteinsCell DifferentiationHumansLymphocyte ActivationT-Lymphocytes, RegulatoryForkhead Transcription FactorsFOXP1 protein, humanRepressor ProteinsantitumorexhaustionFoxP1isoformsquiescenceT cellT cell differentiationTreg

Identifiers

PMID36268015
PMCPMC9576946
OpenAlexW4300819083

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.