Evidence map›Paper›PMID 38489359›Full record

ArticleScience advances2024

Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals.

Laurenz A Herr, Gina J Fiala, Sagar, Anna-Maria Schaffer, Jonas F Hummel, Marina Zintchenko, Katrin Raute, Rubí M-H Velasco Cárdenas, Beate Heizmann, Karolina Ebert and 6 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

16 authors at 3 institutions in 2 countries.

Laurenz A HerrSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.ORCID 0000-0002-1035-2558
Gina J FialaSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.ORCID 0000-0002-8226-5584
SagarDepartment of Medicine II (Gastroenterology, Hepatology, Endocrinology, and Infectious Diseases), Freiburg University Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-8657-4704
Anna-Maria SchafferSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.ORCID 0000-0002-2561-0820
Jonas F HummelInstitute of Medical Microbiology and Hygiene, Medical Center, University of Freiburg, Germany.ORCID 0009-0003-8673-4477
Marina ZintchenkoSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.
Katrin RauteSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.
Rubí M-H Velasco CárdenasSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.
Beate HeizmannInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), INSERM U1258, CNRS UMR7104, Université de Strasbourg, Illkirch, France.ORCID 0000-0002-4236-2937
Karolina EbertInstitute of Medical Microbiology and Hygiene, Medical Center, University of Freiburg, Germany.ORCID 0009-0002-2772-4554
Kerstin FehrenbachSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.
Iga JanowskaSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.ORCID 0009-0004-7526-2803
Susan ChanInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), INSERM U1258, CNRS UMR7104, Université de Strasbourg, Illkirch, France.
Yakup TanriverInstitute of Medical Microbiology and Hygiene, Medical Center, University of Freiburg, Germany.ORCID 0000-0002-4806-2548
Susana MinguetSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.ORCID 0000-0001-8211-5538
Wolfgang W SchamelSignaling Research Centers BIOSS and CIBSS; University of Freiburg, Freiburg, Germany.ORCID 0000-0003-4496-3100
University of Freiburg · DECentre National de la Recherche Scientifique · FRInstitute of Medical Microbiology and Hygiene · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of T cells is controlled by the signal strength of the TCR. The scaffold protein kinase D-interacting substrate of 220 kilodalton (Kidins220) binds to the TCR; however, its role in T cell development was unknown. Here, we show that T cell-specific Kidins220 knockout (T-KO) mice have strongly reduced invariant natural killer T (iNKT) cell numbers and modest decreases in conventional T cells. Enhanced apoptosis due to increased TCR signaling in T-KO iNKT thymocytes of developmental stages 2 and 3 shows that Kidins220 down-regulates TCR signaling at these stages. scRNA-seq  indicated that the transcription factor Aiolos is down-regulated in Kidins220-deficient iNKT cells. Analysis of an Aiolos KO demonstrated that Aiolos is a downstream effector of Kidins220 during iNKT cell development. In the periphery, T-KO iNKT cells show reduced TCR signaling upon stimulation with α-galactosylceramide, suggesting that Kidins220 promotes TCR signaling in peripheral iNKT cells. Thus, Kidins220 reduces or promotes signaling dependent on the iNKT cell developmental stage.

Indexed as

Ikaros Transcription FactorMembrane ProteinsNatural Killer T-CellsThymus GlandAnimalsCell DifferentiationGene Expression RegulationMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-CellSignal TransductionIkaros Transcription FactorIkzf3 protein, mouseKidins220 protein, mouseMembrane ProteinsReceptors, Antigen, T-Cell

Identifiers

PMID38489359
PMCPMC10942104
OpenAlexW4392857158

What OpenQuestion holds

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LicenceCC BY
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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.