Evidence map›Paper›PMID 27258160›Full record

ArticlePloS one2016

CRISPR-Mediated Triple Knockout of SLAMF1, SLAMF5 and SLAMF6 Supports Positive Signaling Roles in NKT Cell Development.

Bonnie Huang, Julio Gomez-Rodriguez, Silvia Preite, Lisa J Garrett, Ursula L Harper, Pamela L Schwartzberg

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
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  4. Development of αβ T Cells with Innate Functions.Advances in experimental medicine and biology · 2022
    Article
  5. Article
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  7. Article
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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

6 authors at 1 institution in 1 country.

Bonnie HuangGenetic Disease Research Branch, National Human Genome Research Institute, Bethesda, Maryland, United States of America.
Julio Gomez-RodriguezGenetic Disease Research Branch, National Human Genome Research Institute, Bethesda, Maryland, United States of America.
Silvia PreiteGenetic Disease Research Branch, National Human Genome Research Institute, Bethesda, Maryland, United States of America.
Lisa J GarrettEmbryonic Stem Cell and Transgenic Mouse Core, National Human Genome Research Institute, Bethesda, Maryland, United States of America.
Ursula L HarperGenomics Core, National Human Genome Research Institute, National Human Genome Research Institute, Bethesda, Maryland, United States of America.
Pamela L SchwartzbergGenetic Disease Research Branch, National Human Genome Research Institute, Bethesda, Maryland, United States of America.
National Human Genome Research Institute · US

Funding

NHGRI/DIR Embryonic Stem Cell and Transgenic Mouse CoreZICHG200349 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BURGESS, SHAWN M · 2010 to 2025
$23.8M
Genetic and Biochemical Approaches to Tyrosine Kinase FunctionZIAHG000123 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SCHWARTZBERG, PAMELA · 2009 to 2018
$20.8M
NHGRI/DIR Genomics CoreZICHG200346 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI CHANDRASEKHARAPPA, SETTARA · 2010 to 2025
$14.5M
Genetic/Biochemical Approaches-Tyrosine Kinase FunctionZ01HG000123 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SCHWARTZBERG, PAMELA · 1998 to 2008
$4.7M
NHGRI/DIR Embryonic Stem Cell and Transgenic Mouse CoreZ01HG200349 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BIESECKER, LESLIE · 2008 to 2008
$1.8M
Intramural NIH HHS Z01 HG000123Intramural NIH HHS Z01 HG200349
6 · The paper itself

Abstract

The SLAM family receptors contribute to diverse aspects of lymphocyte biology and signal via the small adaptor molecule SAP. Mutations affecting SAP lead to X-linked lymphoproliferative syndrome Type 1, a severe immunodysregulation characterized by fulminant mononucleosis, dysgammaglobulinemia, and lymphoproliferation/lymphomas. Patients and mice having mutations affecting SAP also lack germinal centers due to a defect in T:B cell interactions and are devoid of invariant NKT (iNKT) cells. However, which and how SLAM family members contribute to these phenotypes remains uncertain. Three SLAM family members: SLAMF1, SLAMF5 and SLAMF6, are highly expressed on T follicular helper cells and germinal center B cells. SLAMF1 and SLAMF6 are also implicated in iNKT development. Although individual receptor knockout mice have limited iNKT and germinal center phenotypes compared to SAP knockout mice, the generation of multi-receptor knockout mice has been challenging, due to the genomic linkage of the genes encoding SLAM family members. Here, we used Cas9/CRISPR-based mutagenesis to generate mutations simultaneously in Slamf1, Slamf5 and Slamf6. Genetic disruption of all three receptors in triple-knockout mice (TKO) did not grossly affect conventional T or B cell development and led to mild defects in germinal center formation post-immunization. However, the TKO worsened defects in iNKT cells development seen in SLAMF6 single gene-targeted mice, supporting data on positive signaling and potential redundancy between these receptors.

Indexed as

AnimalsB-LymphocytesClustered Regularly Interspaced Short Palindromic RepeatsGerminal CenterLymphocyte ActivationMiceMice, KnockoutNatural Killer T-CellsSignaling Lymphocytic Activation Molecule FamilySignaling Lymphocytic Activation Molecule Family Member 1Signal TransductionT-LymphocytesCd84 protein, mouseSignaling Lymphocytic Activation Molecule FamilySignaling Lymphocytic Activation Molecule Family Member 1Slamf6 protein, mouse

Identifiers

PMID27258160
PMCPMC4892526
OpenAlexW2417592541

What OpenQuestion holds

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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.