Evidence map›Paper›PMID 23416161›Full record

ArticleThe American journal of pathology2013

CD44 deficiency contributes to enhanced experimental autoimmune encephalomyelitis: a role in immune cells and vascular cells of the blood-brain barrier.

Kelly M Flynn, Michael Michaud, Joseph A Madri

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.6field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
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  8. Protective Effects of Luteolin onAntibiotics (Basel, Switzerland) · 2025
    Article
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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

3 authors at 1 institution in 1 country.

Kelly M FlynnDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520-8023, USA.
Michael Michaud
Joseph A Madri
Yale University · US

Funding

Skill Development for Diverse Scientific Careers: A New Course Predoctoral Program in Cellular and Molecular BiologyT32GM007223 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 1985 to 2019
$31.0M
PATHOLOGY OF ENDOTHELIAL NEOVASCULARIZATIONR37HL028373 · NHLBI · YALE UNIVERSITY · PI MADRI, JOSEPH A · 1999 to 2008
$4.6M
PROTEINASE MODULATION DURING T CELL-ENDOTHELIAL ADHESIONR01HL051018 · NHLBI · YALE UNIVERSITY · PI MADRI, JOSEPH A · 1995 to 2010
$3.1M
EXPERIMENTAL AND HUMAN PATHOBIOLOGYT32DK007556 · NIDDK · YALE UNIVERSITY · PI MORROW, JON S · 1987 to 2011
$2.6M
NHLBI NIH HHS R01 HL051018NHLBI NIH HHS R01-HL51018NHLBI NIH HHS R37 HL028373NHLBI NIH HHS R37-HL28373NIDDK NIH HHS T32 DK007556NIDDK NIH HHS T32 DK07556NIGMS NIH HHS T32 GM007223
6 · The paper itself

Abstract

Adhesion molecule CD44 is expressed by multiple cell types and is implicated in various cellular and immunological processes. In this study, we examined the effect of global CD44 deficiency on myelin oligodendrocyte glycoprotein peptide (MOG)-induced experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. Compared to C57BL/6 wild-type mice, CD44-deficient mice presented with greater disease severity, increased immune cell numbers in the central nervous system, and increased anti-MOG antibody and proinflammatory cytokine production, especially those associated with T helper 17 (Th17) cells. Further, decreased numbers of peripheral CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tregs) were observed in CD44-knockout mice throughout the disease course. CD44-knockout CD4 T cells exhibited reduced transforming growth factor-β receptor type I (TGF-β RI) expression that did not impart a defect in Treg polarization in vitro, but did correlate with enhanced Th17 polarization in vitro. Further, EAE in bone marrow-chimeric animals suggested CD44 expression on both circulating and noncirculating cells limited disease severity. Endothelial expression of CD44 limited T-cell adhesion to and transmigration through murine endothelial monolayers in vitro. Importantly, we also identified increased permeability of the blood-brain barrier in vivo in CD44-deficient mice before and following immunization. These data suggest that CD44 has multiple protective roles in EAE, with effects on cytokine production, T-cell differentiation, T-cell-endothelial cell interactions, and blood-brain barrier integrity.

Indexed as

AnimalsBlood-Brain BarrierBone Marrow CellsCell AdhesionCell MovementCell PolarityChimeraEncephalomyelitis, Autoimmune, ExperimentalEndothelial CellsGene DeletionHyaluronan ReceptorsInflammationInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutHyaluronan ReceptorsInflammation MediatorsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type I

Identifiers

PMID23416161
PMCPMC3620422
OpenAlexW1855077198

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.