Evidence map›Paper›PMID 26673421›Full record

ArticlePloS one2015

MicroRNA-181a/b-1 Is Not Required for Innate γδ NKT Effector Cell Development.

Inga Sandrock, Natalia Ziętara, Marcin Łyszkiewicz, Linda Oberdörfer, Katrin Witzlau, Andreas Krueger, Immo Prinz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  3. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
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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

7 authors at 1 institution in 1 country.

Inga SandrockInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Natalia ZiętaraInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Marcin ŁyszkiewiczInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Linda OberdörferInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Katrin WitzlauInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Andreas KruegerInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Immo PrinzInstitute of Immunology, Hannover Medical School, 30625 Hannover, Germany.
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thymic development of αβ T lymphocytes into invariant natural killer (NK) T cells depends on their selection via agonistic lipid antigen presented by CD1d. If successful, newly selected NKT cells gain effector functions already in the thymus. Some γδ T cell subsets also acquire effector functions in the thymus. However, it is not clear whether agonistic TCR stimulation is involved in thymic γδ T cell selection and development. Here we combine two genetic models to address this question. MiR-181a/b-1-/-mice, which show impaired agonistic T cell selection of invariant αβ NKT cells, were crossed to Tcrd-H2BeGFP reporter mice to monitor selection, intra-thymic expansion and differentiation of γδ T cells. We found that miR-181a/b-1-deficiency had no effect on numbers of thymic γδ T cell or on their differentiation towards an IL-17- or IFN-γ-producing effector phenotype. Also, the composition of peripheral lymph node γδ T cells was not affected by miR-181a/b-1-deficiency. Dendritic epidermal γδ T cells were normally present in knock-out animals. However, we observed elevated frequencies and numbers of γδ NKT cells in the liver, possibly because γδ NKT cells can expand and replace missing αβ NKT cells in peripheral niches. In summary, we investigated the role of miR-181a/b-1 for selection, intrathymic development and homeostasis of γδ T cells. We conclude that miR-181a/b-1-dependent modulation of T cell selection is not critically required for innate development of γδ NKT cells or of any other γδ T cell subtypes.

Indexed as

Immunity, InnateAnimalsAntigens, CD1dCell DifferentiationClonal Selection, Antigen-MediatedImmunophenotypingLiverLymph NodesMiceMice, KnockoutMice, TransgenicMicroRNAsNatural Killer T-CellsPhenotypeReceptors, Antigen, T-Cell, gamma-deltaT-Cell Antigen Receptor SpecificityAntigens, CD1dMicroRNAsmirn181 microRNA, mouseReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID26673421
PMCPMC4682956
OpenAlexW2198348811

What OpenQuestion holds

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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.