Evidence map›Paper›PMID 38565808›Full record

ArticleCellular and molecular life sciences : CMLS2024

Positive regulation of Vav1 by Themis controls CD4 T cell pathogenicity in a mouse model of central nervous system inflammation.

Remi Marrocco, Isabelle Bernard, Emeline Joulia, Rebecca Barascud, Anne S Dejean, Renaud Lesourne, Abdelhadi Saoudi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. 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

7 authors at 1 institution in 2 countries.

Remi MarroccoInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France.
Isabelle BernardInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France.
Emeline JouliaInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France.
Rebecca BarascudInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France.
Anne S DejeanInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France.
Renaud LesourneInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France.
Abdelhadi SaoudiInstitut Toulousain des Maladies Infectieuses Et Inflammatoires (Infinity), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), INSERM U1291, Université Paul Sabatier (UPS), CHU Purpan, BP 3028, 31024, Toulouse Cedex 3, France. abdelhadi.saoudi@inserm.fr.ORCID http://orcid.org/0000-0001-7015-8178
Centre National de la Recherche Scientifique · FR

Funding

Agence Nationale de la Recherche ANR-20-CE15-0005-01
6 · The paper itself

Abstract

The susceptibility to autoimmune diseases is conditioned by the association of modest genetic alterations which altogether weaken self-tolerance. The mechanism whereby these genetic interactions modulate T-cell pathogenicity remains largely uncovered. Here, we investigated the epistatic interaction of two interacting proteins involved in T Cell Receptor signaling and which were previously associated with the development of Multiple Sclerosis. To this aim, we used mice expressing an hypomorphic variant of Vav1 (Vav1

Indexed as

CD4-Positive T-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalAnimalsCentral Nervous SystemHumansInflammationIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLProto-Oncogene Proteins c-vavVirulenceIntercellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-vavthemis protein, mouseVav1 protein, mouseAutoimmunityEpistasisSignalingSusceptibility geneTCR

Identifiers

PMID38565808
PMCPMC10987373
OpenAlexW4393561601

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.