Evidence map›Paper›PMID 22529957›Full record

ArticlePloS one2012

Tuftsin promotes an anti-inflammatory switch and attenuates symptoms in experimental autoimmune encephalomyelitis.

Muzhou Wu, Jillian C Nissen, Emily I Chen, Stella E Tsirka

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.4field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Muzhou WuDepartment of Pharmacological Sciences, School of Medicine, Stony Brook University, Stony Brook, New York, United States of America.
Jillian C Nissen
Emily I Chen
Stella E Tsirka
Stony Brook University · US

Funding

Training Program in Pharmacological SciencesT32GM007518 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI GARCIA-DIAZ, MIGUEL · 1985 to 2021
$5.4M
Microglial effector pathways in the CNSR01NS042168 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI TSIRKA, STYLIANI-ANNA (STELLA) E · 2003 to 2011
$3.1M
Acquisition of an Applied Biosystems 4000 QTRAP Mass SpectrometerS10RR023680 · NCRR · STATE UNIVERSITY NEW YORK STONY BROOK · PI IDEN, CHARLES R · 2007 to 2007
$435k
NCI NIH HHS CA1044A1NCRR NIH HHS 1 S10 RR023680-1NCRR NIH HHS S10 RR023680NIGMS NIH HHS T32 GM007518NINDS NIH HHS R01 NS042168NINDS NIH HHS R01NS42168
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 T cell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS.

Indexed as

Adoptive TransferAnimalsCulture Media, ConditionedDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalFemaleForkhead Transcription FactorsImmunologic FactorsImmunosuppression TherapyMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMicrogliaPhenotypeSignal TransductionCulture Media, ConditionedForkhead Transcription FactorsFoxp3 protein, mouseImmunologic FactorsSTAT1 Transcription FactorTuftsin

Identifiers

PMID22529957
PMCPMC3328491
OpenAlexW1992765482

What OpenQuestion holds

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LicenceCC BY
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.