Evidence map›Paper›PMID 23261777›Full record

ArticleBrain, behavior, and immunity2013

Higher susceptibility to experimental autoimmune encephalomyelitis in Muc1-deficient mice is associated with increased Th1/Th17 responses.

Jui-Hung Yen, Shuyun Xu, Yong Sung Park, Doina Ganea, Kwang Chul Kim

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 41% 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, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. MUC1: Structure, Function, and Clinic Application in Epithelial Cancers.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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

5 authors at 1 institution in 1 country.

Jui-Hung YenDepartment of Microbiology & Immunology and Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, PA, United States.
Shuyun XuDepartment of Microbiology & Immunology and Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, PA, United States.
Yong Sung ParkDepartment of Microbiology & Immunology and Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, PA, United States.
Doina GaneaDepartment of Microbiology & Immunology and Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, PA, United States.
Kwang Chul KimDepartment of Microbiology & Immunology and Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, PA, United States. Electronic address: kckim@temple.edu.
Temple University · US

Funding

SIGNALING MECHANISM OF MUC1 MUCINR01HL047125 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI KIM, KWANG CHUL · 1991 to 2015
$4.5M
CB2 Receptor Regulatin of Inflammatory Response in EAER01AI084065 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GANEA, DOINA, TUMA, RONALD F · 2009 to 2012
$1.5M
ROLE OF MUC1 IN THE GENESIS OF ALLERGIC ASTHMAR21AI073988 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI KIM, KWANG CHUL · 2009 to 2010
$413k
NHLBI NIH HHS R01 HL047125NHLBI NIH HHS R01 HL47125NIAID NIH HHS R01 AI084065NIAID NIH HHS R21 AI073988
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system in which dendritic cells (DC) play an important role in the development of inflammatory responses. Recently it has been shown that Muc1, a membrane tethered glycoprotein, has an ability to suppress inflammatory responses in cultured DC. The objective of this study was to investigate the possible involvement of Muc1 in the development of MS using experimental autoimmune encephalomyelitis (EAE) in mice, a widely used animal model of MS. Our results showed that: (1) Muc1(-/-) mice developed greater EAE severity compared with wild type (wt) mice, which correlated with increased numbers of Th1 and Th17 cells infiltrating into the CNS; (2) upon stimulation, splenic DC from Muc1(-/-) mice produced greater amounts of IL-1β, IL-6, and IL-12 but less amounts of IL-10 compared with those from wt mice; and (3) the ability of splenic DC to differentiate antigen-specific CD4+ T cells into Th1 and Th17 cells was greater in Muc1(-/-) mice compared with wt mice. We conclude that Muc1 plays an anti-inflammatory role in EAE. This is the first report demonstrating the possible involvement of Muc1 in the development of MS and might provide a potential target for immunotherapy.

Indexed as

AnimalsCD4-Positive T-LymphocytesCells, CulturedCell SeparationCentral Nervous SystemDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryInterleukinsMiceMice, Inbred C57BLMice, KnockoutMucin-1Multiple SclerosisInterleukinsMucin-1

Identifiers

PMID23261777
PMCPMC3587144
OpenAlexW2146470906

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.