Evidence map›Paper›PMID 24591371›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Relapsing-remitting central nervous system autoimmunity mediated by GFAP-specific CD8 T cells.

Katsuhiro Sasaki, Angela Bean, Shivanee Shah, Elizabeth Schutten, Priya G Huseby, Bjorn Peters, Zu T Shen, Vijay Vanguri, Denny Liggitt, Eric S Huseby

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.2field-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

69 citing papers in PubMed, 112 citations in OpenAlex.

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  16. Life history of a brain autoreactive T cell: From thymus through intestine to blood-brain barrier and brain lesion.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. IL-21, not IL-17A, exacerbates murine primary biliary cholangitis.Clinical and experimental immunology · 2024
    Article

9 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Katsuhiro SasakiDepartment of Pathology, University of Massachusetts Medical School, Worcester, MA 01655;
Angela Bean
Shivanee Shah
Elizabeth Schutten
Priya G Huseby
Bjorn Peters
Zu T Shen
Vijay Vanguri
Denny Liggitt
Eric S Huseby
University of Massachusetts Chan Medical School · USLa Jolla Institute for Immunology · USUniversity of Washington · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
TRAINING IN IMMUNOLOGY (COMPETITIVE RENEWAL OF AI07439)T32AI007349 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STERN, LAWRENCE J. · 1989 to 2024
$4.5M
Origin and Control of Self-Reactive TCRsR01DK095077 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HUSEBY, ERIC S · 2012 to 2016
$1.8M
Inflammatory and Suppressive mechanisms of CNS autoimmunityR21AI088495 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HUSEBY, ERIC S · 2010 to 2011
$409k
NIAID NIH HHS R21 AI088495NIAID NIH HHS T32 AI007349NIDDK NIH HHS DK095077NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520NIDDK NIH HHS R01 DK095077PHS HHS RAI088495A
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory disease of the CNS that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons, and axons. Historically, MS has been thought to be a CD4 T cell-mediated autoimmune disease of CNS white matter. However, recent studies identified CD8 T cell infiltrates and gray matter lesions in MS patients. These findings suggest that CD8 T cells and CNS Ags other than myelin proteins may be involved during the MS disease process. In this article, we show that CD8 T cells reactive to glial fibrillary acidic protein (GFAP), a protein expressed in astrocytes, can avoid tolerance mechanisms and, depending upon the T cell-triggering event, drive unique aspects of inflammatory CNS autoimmunity. In GFAP-specific CD8 TCR-transgenic (BG1) mice, tissue resident memory-like CD8 T cells spontaneously infiltrate the gray matter and white matter of the CNS, resulting in a relapsing-remitting CNS autoimmunity. The frequency, severity, and remissions from spontaneous disease are controlled by the presence of polyclonal B cells. In contrast, a viral trigger induces GFAP-specific CD8 T effector cells to exclusively target the meninges and vascular/perivascular space of the gray and white matter of the brain, causing a rapid, acute CNS disease. These findings demonstrate that the type of CD8 T cell-triggering event can determine the presentation of distinct CNS autoimmune disease pathologies.

Indexed as

AnimalsAstrocytesAutoimmunityBrainCD8-Positive T-LymphocytesCells, CulturedCentral Nervous SystemCentral Nervous System DiseasesFlow CytometryGlial Fibrillary Acidic ProteinImmunohistochemistryInterferon-gammaMiceMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutGlial Fibrillary Acidic ProteinInterferon-gammaReceptors, Antigen, T-Cell

Identifiers

PMID24591371
PMCPMC3967518
OpenAlexW2111501033

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.