Evidence map›Paper›PMID 29985916›Full record

ArticlePLoS biology2018

The actin remodeling protein cofilin is crucial for thymic αβ but not γδ T-cell development.

Isabel Seeland, Ying Xiong, Christian Orlik, Daniel Deibel, Sandra Prokosch, Günter Küblbeck, Beate Jahraus, Daniela De Stefano, Sonja Moos, Florian C Kurschus and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. γδ T Cells and Inborn Errors of Immunity.European journal of immunology · 2025
    Review
  2. Review
  3. Inactivation of cofilin-1 in Mcpt5-Cre-nf-Cfl1Frontiers in immunology · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
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

12 authors at 3 institutions in 1 country.

Isabel SeelandInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Ying XiongInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Christian OrlikInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Daniel DeibelInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Sandra ProkoschInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Günter KüblbeckFormer Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Beate JahrausInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Daniela De StefanoInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Sonja MoosInstitute of Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Florian C KurschusInstitute of Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Bernd ArnoldFormer Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Yvonne SamstagInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Heidelberg University · DEJohannes Gutenberg University Mainz · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cofilin is an essential actin remodeling protein promoting depolymerization and severing of actin filaments. To address the relevance of cofilin for the development and function of T cells in vivo, we generated knock-in mice in which T-cell-specific nonfunctional (nf) cofilin was expressed instead of wild-type (WT) cofilin. Nf cofilin mice lacked peripheral αβ T cells and showed a severe thymus atrophy. This was caused by an early developmental arrest of thymocytes at the double negative (DN) stage. Importantly, even though DN thymocytes expressed the TCRβ chain intracellularly, they completely lacked TCRβ surface expression. In contrast, nf cofilin mice possessed normal numbers of γδ T cells. Their functionality was confirmed in the γδ T-cell-driven, imiquimod (IMQ)-induced, psoriasis-like murine model. Overall, this study not only highlights the importance of cofilin for early αβ T-cell development but also shows for the first time that an actin-binding protein is differentially involved in αβ versus γδ T-cell development.

Indexed as

Actin Depolymerizing FactorsActinsAnimalsCell MovementGene Knock-In TechniquesHumansJurkat CellsMiceMutationProlineReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaThymocytesThymus GlandT-LymphocytesT-Lymphocyte SubsetsActin Depolymerizing FactorsActinsProlineReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID29985916
PMCPMC6053251
OpenAlexW2854037000

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.