Evidence map›Paper›PMID 24435747›Full record

ArticleEuropean journal of immunology2014

Expression of a single ICAM-1 isoform on T cells is sufficient for development of experimental autoimmune encephalomyelitis.

Daniel C Bullard, Xianzhen Hu, David Crawford, Kristin McDonald, Theresa N Ramos, Scott R Barnum

Abstract read
In one paragraph

Article in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. The IL-27/IL-27R axis is altered in CD4Clinical & translational immunology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. ICAM-1: isoforms and phenotypes.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
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

6 authors at 2 institutions in 1 country.

Daniel C BullardDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL, USA.
Xianzhen Hu
David Crawford
Kristin McDonald
Theresa N Ramos
Scott R Barnum
University of Alabama at Birmingham · USOklahoma City University · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
UAB Recessive PKD Research and Translational Core CenterP30DK074038 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 2005 to 2019
$16.6M
IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
UAB Diabetes Research and Training CenterP60DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 2008 to 2012
$8.4M
The Role of C3 and C3 receptors in Experimental Autoimmune EncephalomyelitisR01NS046032 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNUM, SCOTT R · 2004 to 2007
$1.2M
The role of the terminal complement pathway in experimental cerebral malaria.F31NS077811 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAMOS, THERESA N · 2012 to 2012
$24k
NCI NIH HHS P30 CA013148NCI NIH HHS P30 CA13148NIAID NIH HHS T32 AI007051NIAMS NIH HHS P30 AR048311NIDDK NIH HHS P30 DK05336NIDDK NIH HHS P30 DK074038NIDDK NIH HHS P60 DK079626NINDS NIH HHS F31 NS077811NINDS NIH HHS R01 NS046032
6 · The paper itself

Abstract

Intercellular adhesion molecule-1 (ICAM-1) plays an important role in leukocyte trafficking, induction of cellular immune responses, and immunological synapse formation. As a member of the immunoglobulin superfamily of adhesion proteins, ICAM-1 is composed of repeating Ig-like domains, a transmembrane domain, and short cytoplasmic tail that participates in intracellular signaling events. At least seven ICAM-1 protein isoforms are generated by alternative splicing, however little is known regarding their immunobiology. We have previously shown using different lines of ICAM-1 mutant mice (Icam1(tm1Jcgr) and Icam1(tm1Bay) ) that expression of alternatively spliced ICAM-1 isoforms can significantly influence the disease course during the development of EAE. In this study, we show using a newly developed transgenic mouse (CD2-Icam1(D4del) /Icam1(null) ) that T-cell-specific expression of a single ICAM-1 isoform composed of Ig domains 1, 2, 3, and 5 can mediate the initiation and progression of EAE. Our results indicate that the ICAM-1 isoform lacking Ig domain 4 can drive pathogenesis in demyelinating disease and may be a novel therapeutic target for treating multiple sclerosis.

Indexed as

Adoptive TransferAlternative SplicingAnimalsBinding SitesBlotting, WesternEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryHEK293 CellsHumansIntercellular Adhesion Molecule-1MiceMice, KnockoutMice, TransgenicProtein IsoformsT-LymphocytesIntercellular Adhesion Molecule-1Protein IsoformsAdhesion moleculesAlternative splicingCentral nervous systemDemyelinating diseaseTransgenic animals

Identifiers

PMID24435747
PMCPMC3984619
OpenAlexW1528462206

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.