Evidence map›Paper›PMID 25569805›Full record

ArticleMolecular medicine (Cambridge, Mass.)2015

Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion.

Prameladevi Chinnasamy, Sarah E Lutz, Dario F Riascos-Bernal, Venkatesh Jeganathan, Isabel Casimiro, Celia F Brosnan, Nicholas E S Sibinga

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  10. Altered synaptic connectivity and brain function in mice lacking microglial adapter protein Iba1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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  14. TGF-β-mediated enhancement of TScience signaling · 2018
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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

7 authors at 2 institutions in 1 country.

Prameladevi ChinnasamyDepartment of Medicine (Cardiovascular Division), Albert Einstein College of Medicine, Bronx, New York, United States of America.
Sarah E LutzDepartment of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, United States of America.
Dario F Riascos-BernalDepartment of Medicine (Cardiovascular Division), Albert Einstein College of Medicine, Bronx, New York, United States of America.
Venkatesh JeganathanCenter for Autoimmune and Musculoskeletal Disease, The Feinstein Institute of Medical Research, Manhasset, New York, United States of America.
Isabel CasimiroDepartment of Medicine (Cardiovascular Division), Albert Einstein College of Medicine, Bronx, New York, United States of America.
Celia F BrosnanDepartment of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, United States of America.
Nicholas E S SibingaDepartment of Medicine (Cardiovascular Division), Albert Einstein College of Medicine, Bronx, New York, United States of America.
Albert Einstein College of Medicine · USFeinstein Institute for Medical Research · US

Funding

Allograft Inflammatory Factor in Transplant VasculopathyR01HL067944 · NHLBI · YESHIVA UNIVERSITY · PI SIBINGA, NICHOLAS E · 2002 to 2005
$1.5M
NHLBI NIH HHS HL67944NHLBI NIH HHS R01 HL067944
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), is mediated by myelin-specific autoreactive T cells that cause inflammation and demyelination in the central nervous system (CNS), with significant contributions from activated microglia and macrophages. The molecular bases for expansion and activation of these cells, plus trafficking to the CNS for peripheral cells, are not fully understood. Allograft inflammatory factor-1 (Aif-1) (also known as ionized Ca(2+) binding adapter-1 [Iba-1]) is induced in leukocytes in MS and EAE; here we provide the first assessment of Aif-1 function in this setting. After myelin oligodendrocyte glycoprotein peptide (MOG35-55) immunization, Aif-1-deficient mice were less likely than controls to develop EAE and had less CNS leukocyte infiltration and demyelination; their spinal cords contained fewer CD4 T cells and microglia and more CD8 T cells. These mice also showed significantly less splenic CD4 T-cell expansion and activation, plus decreased proinflammatory cytokine expression. These findings identify Aif-1 as a potent molecule that promotes expansion and activation of CD4 T cells, plus elaboration of a proinflammatory cytokine milieu, in MOG35-55-induced EAE and as a potential therapeutic target in MS.

Indexed as

AnimalsCalcium-Binding ProteinsCD4-Positive T-LymphocytesDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalLeukocytesLymphocyte ActivationMiceMice, KnockoutMicrofilament ProteinsSeverity of Illness IndexSpleenT-Lymphocyte SubsetsAif1 protein, mouseCalcium-Binding ProteinsMicrofilament Proteins

Identifiers

PMID25569805
PMCPMC4503655
OpenAlexW2415106056

What OpenQuestion holds

Textmetadata
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.