Evidence map›Paper›PMID 19915062›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

SLAT/Def6 plays a critical role in the development of Th17 cell-mediated experimental autoimmune encephalomyelitis.

Ann J Canonigo-Balancio, Camille Fos, Thomas Prod'homme, Stéphane Bécart, Amnon Altman

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

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  18. Expression of IRF-4 and IBP in skin lesions of patients with psoriasis vulgaris.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2012
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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

5 authors at 2 institutions in 1 country.

Ann J Canonigo-BalancioDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Camille Fos
Thomas Prod'homme
Stéphane Bécart
Amnon Altman
La Jolla Institute for Immunology · USUniversity of California, San Francisco · US

Funding

SLAT: A novel GEF coordinating actin remodeling and Ca2+ signaling in T cellsR01AI068320 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI ALTMAN, AMNON · 2006 to 2015
$4.5M
NIAID NIH HHS AI68320NIAID NIH HHS R01 AI068320
6 · The paper itself

Abstract

SWAP-70-like adapter of T cells (SLAT; also known as Def6) is a novel guanine nucleotide exchange factor for Rho GTPases that has been previously shown to play a role in CD4+ T cell activation and Th1/Th2 differentiation. However, the role of SLAT/Def6 in autoimmunity and its associated Th1- and Th17-specific responses has not yet been clearly elucidated. We used a prototypical and pathologically relevant Th1/Th17-mediated autoimmune model, that is, experimental autoimmune encephalomyelitis, to assess the role of SLAT/Def6 in autoantigen-specific T cell response. We found that T cell-expressed SLAT/Def6 was critical for experimental autoimmune encephalomyelitis development and pathogenesis, as evidenced by the resistance of Def6-deficient (Def6(-/-)) mice to clinical signs of the disease associated with a lack of CNS inflammation and demyelination in myelin oligodendrocyte glycoprotein-immunized Def6(-/-) mice. Moreover, Def6 deficiency resulted in a severely diminished myelin oligodendrocyte glycoprotein-specific CD4+ T cell proliferation as well as a defect in IFN-gamma and IL-17 production in secondary lymphoid organs and the CNS. Lastly, Def6(-/-) CD4+ T cells were grossly deficient in their ability to differentiate into Th17 cells both in vitro and in vivo in a T cell-intrinsic manner. Therefore, our study establishes T cell-expressed SLAT/Def6 as a pivotal positive regulator of Th17 inflammatory responses and, thus, essential in controlling autoimmune and inflammatory diseases.

Indexed as

Adoptive TransferAnimalsCD4-Positive T-LymphocytesCell DifferentiationDNA-Binding ProteinsEncephalomyelitis, Autoimmune, ExperimentalGuanine Nucleotide Exchange FactorsInterleukin-17MiceMice, KnockoutNuclear ProteinsT-Lymphocyte SubsetsDef6 protein, mouseDNA-Binding ProteinsGuanine Nucleotide Exchange FactorsInterleukin-17Nuclear Proteins

Identifiers

PMID19915062
PMCPMC2821872
OpenAlexW2167511285

What OpenQuestion holds

Textmetadata
LicenceTDM
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.