Evidence map›Paper›PMID 25573673›Full record

ArticleScientific reports2015

Distinct p21 requirements for regulating normal and self-reactive T cells through IFN-γ production.

Lidia Daszkiewicz, Cristina Vázquez-Mateo, Gorjana Rackov, André Ballesteros-Tato, Kathrin Weber, Adrián Madrigal-Avilés, Mauro Di Pilato, Arun Fotedar, Rati Fotedar, Juana M Flores and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
0.8field-weighted citation impact, top 28% 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, 26 citations in OpenAlex.

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  10. Lack of Cell Cycle Inhibitor p21 and Low CD4Frontiers in immunology · 2021
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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

13 authors at 5 institutions in 2 countries.

Lidia DaszkiewiczDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Cristina Vázquez-MateoDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Gorjana RackovDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
André Ballesteros-TatoDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Kathrin WeberDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Adrián Madrigal-AvilésDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Mauro Di PilatoDepartment of Cellular and Molecular Biology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Arun FotedarCancer Cell Biology Program, Sidney Kimmel Cancer Center, San Diego, CA, USA.
Rati FotedarSanford-Burnham Medical Research Institute, San Diego, CA, USA.
Juana M FloresAnimal Biology Department, School of Veterinary Medicine, Universidad Complutense, Madrid, Spain.
Mariano EstebanDepartment of Cellular and Molecular Biology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Carlos Martínez-ADepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Dimitrios BalomenosDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain.
Consejo Superior de Investigaciones Científicas · ESUniversidad Autónoma de Madrid · ESSanford Burnham Prebys Medical Discovery Institute · USSidney Kimmel Cancer Center · USUniversidad Complutense de Madrid · ES

Funding

NIMHD NIH HHS L60 MD002502
6 · The paper itself

Abstract

Self/non-self discrimination characterizes immunity and allows responses against pathogens but not self-antigens. Understanding the principles that govern this process is essential for designing autoimmunity treatments. p21 is thought to attenuate autoreactivity by limiting T cell expansion. Here, we provide direct evidence for a p21 role in controlling autoimmune T cell autoreactivity without affecting normal T cell responses. We studied C57BL/6, C57BL/6/lpr and MRL/lpr mice overexpressing p21 in T cells, and showed reduced autoreactivity and lymphadenopathy in C57BL/6/lpr, and reduced mortality in MRL/lpr mice. p21 inhibited effector/memory CD4(+) CD8(+) and CD4(-)CD8(-) lpr T cell accumulation without altering defective lpr apoptosis. This was mediated by a previously non-described p21 function in limiting T cell overactivation and overproduction of IFN-γ, a key lupus cytokine. p21 did not affect normal T cell responses, revealing differential p21 requirements for autoreactive and normal T cell activity regulation. The underlying concept of these findings suggests potential treatments for lupus and autoimmune lymphoproliferative syndrome, without compromising normal immunity.

Indexed as

AnimalsApoptosisAutoimmune DiseasesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Immunologic MemoryInterferon-gammaLymphocyte ActivationMiceMice, Inbred C57BLMice, Inbred MRL lprOvalbuminT-LymphocytesCyclin-Dependent Kinase Inhibitor p21Interferon-gammaOvalbumin

Identifiers

PMID25573673
PMCPMC4287747
OpenAlexW2047394198

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.