Evidence map›Paper›PMID 20348424›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Central nervous system destruction mediated by glutamic acid decarboxylase-specific CD4+ T cells.

Amanda R Burton, Zachary Baquet, George S Eisenbarth, Roland Tisch, Richard Smeyne, Creg J Workman, Dario A A Vignali

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 73 citations in OpenAlex.

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  16. Review
  17. Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect.International journal of molecular sciences · 2020
    Review
  18. Review
  19. Neurological Syndromes Associated with Anti-GAD Antibodies.International journal of molecular sciences · 2020
    Review
  20. 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 3 institutions in 1 country.

Amanda R BurtonDepartment of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105-3678, USA.
Zachary Baquet
George S Eisenbarth
Roland Tisch
Richard Smeyne
Creg J Workman
Dario A A Vignali
St. Jude Children's Research Hospital · USUniversity of Colorado Health · USUniversity of North Carolina at Chapel Hill · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Virginia Mason/UCHSC Autoimmune Prevention CenterU19AI050864 · NIAID · UNIVERSITY OF COLORADO DENVER · PI EISENBARTH, GEORGE S · 2001 to 2011
$29.2M
Control of CD4+ T cell Islet Entry and DiabetogenicityR56AI072239 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI VIGNALI, DARIO AA · 2008 to 2008
$418k
NCI NIH HHS CA-21765NCI NIH HHS P30 CA021765NIAID NIH HHS AI072239NIAID NIH HHS R56 AI072239NIAID NIH HHS U19 AI050864
6 · The paper itself

Abstract

High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells in type 1 diabetes, little is known about their role in SPS. In this study, we show that mice possessing a monoclonal GAD65-specific CD4(+) T cell population (4B5, PA19.9G11, or PA17.9G7) develop a lethal encephalomyelitis-like disease in the absence of any other T cells or B cells. GAD65-reactive CD4(+) T cells were found throughout the CNS in direct concordance with GAD65 expression and activated microglia: proximal to the circumventricular organs at the interface between the brain parenchyma and the blood-brain barrier. In the presence of B cells, high titer anti-GAD65 autoantibodies were generated, but these had no effect on the incidence or severity of disease. In addition, GAD65-specific CD4(+) T cells isolated from the brain were activated and produced IFN-gamma. These findings suggest that GAD65-reactive CD4(+) T cells alone mediate a lethal encephalomyelitis-like disease that may serve as a useful model to study GAD65-mediated diseases of the CNS.

Indexed as

AnimalsAutoantibodiesB-LymphocytesCD4-Positive T-LymphocytesCell MovementClone CellsCytokinesDiabetes Mellitus, Type 1EncephalomyelitisEpitopes, T-LymphocyteFemaleGlutamate DecarboxylaseImmunophenotypingInflammation MediatorsMiceMice, Inbred NODAutoantibodiesCytokinesEpitopes, T-LymphocyteGlutamate Decarboxylaseglutamate decarboxylase 2Inflammation MediatorsReceptors, Antigen, T-Cell

Identifiers

PMID20348424
PMCPMC2989406
OpenAlexW2125989828

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.