Evidence map›Paper›PMID 24277699›Full record

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

Eliminating encephalitogenic T cells without undermining protective immunity.

Jonathan P McNally, Eileen E Elfers, Catherine E Terrell, Eli Grunblatt, David A Hildeman, Michael B Jordan, Jonathan D Katz

Erratum issuedOpen access · greenAbstract 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. An erratum has been issued. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  5. Review
  6. Review
  7. Article
  8. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jonathan P McNallyDivision of Immunobiology, Cincinnati Children's Research Foundation, Cincinnati, OH 45229;
Eileen E Elfers
Catherine E Terrell
Eli Grunblatt
David A Hildeman
Michael B Jordan
Jonathan D Katz
Cincinnati Children's Hospital Medical Center · USHospital Research Foundation · AUUniversity of Cincinnati Medical Center · US

Funding

ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI THOMPSON, SUSAN D · 2001 to 2015
$9.2M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
Dissecting Dendritic Cell Function in Autoimmune DiabetesR01DK078179 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI KATZ, JONATHAN DAVID · 2009 to 2013
$1.7M
Control of Diabetes by Manipulation of Bc12 Family MembersR01DK081175 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI HILDEMAN, DAVID A, KATZ, JONATHAN DAVID · 2011 to 2014
$1.4M
NIAMS NIH HHS P30 AR047363NIDDK NIH HHS P30 DK090971NIDDK NIH HHS R01 DK078179NIDDK NIH HHS R01 DK081175
6 · The paper itself

Abstract

The current clinical approach for treating autoimmune diseases is to broadly blunt immune responses as a means of preventing autoimmune pathology. Among the major side effects of this strategy are depressed beneficial immunity and increased rates of infections and tumors. Using the experimental autoimmune encephalomyelitis model for human multiple sclerosis, we report a novel alternative approach for purging autoreactive T cells that spares beneficial immunity. The moderate and temporally limited use of etoposide, a topoisomerase inhibitor, to eliminate encephalitogenic T cells significantly reduces the onset and severity of experimental autoimmune encephalomyelitis, dampens cytokine production and overall pathology, while dramatically limiting the off-target effects on naive and memory adaptive immunity. Etoposide-treated mice show no or significantly ameliorated pathology with reduced antigenic spread, yet have normal T cell and T-dependent B cell responses to de novo antigenic challenges as well as unimpaired memory T cell responses to viral rechallenge. Thus, etoposide therapy can selectively ablate effector T cells and limit pathology in an animal model of autoimmunity while sparing protective immune responses. This strategy could lead to novel approaches for the treatment of autoimmune diseases with both enhanced efficacy and decreased treatment-associated morbidities.

Indexed as

Lymphocyte DepletionAnimalsApoptosisB-LymphocytesCD4-Positive T-LymphocytesDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalEtoposideFemaleImmunologic MemoryLymphocyte ActivationLymphocytic choriomeningitis virusMiceMultiple SclerosisRecurrenceT-LymphocytesEtoposide

Identifiers

PMID24277699
PMCPMC3872266
OpenAlexW2100049814

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.