Evidence map›Paper›PMID 24600555›Full record

ArticleResults in immunology2013

Tollip-induced down-regulation of MARCH1.

Marie-Claude Bourgeois-Daigneault, Abdul Mohammad Pezeshki, Tristan Galbas, Mathieu Houde, Martin Baril, Klaus Früh, Abdelaziz Amrani, Satoshi Ishido, Daniel Lamarre, Jacques Thibodeau

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Results in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 15 citations in OpenAlex.

  1. TOLLIP Optimizes Dendritic Cell Maturation to Lipopolysaccharide andJournal of immunology (Baltimore, Md. : 1950) · 2022
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  3. Review
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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

10 authors at 5 institutions in 3 countries.

Marie-Claude Bourgeois-DaigneaultLaboratoire d'Immunologie Moléculaire, Département de Microbiologie et Immunologie, Université de Montréal, QC, Canada.
Abdul Mohammad PezeshkiLaboratoire d'Immunologie Moléculaire, Département de Microbiologie et Immunologie, Université de Montréal, QC, Canada.
Tristan GalbasLaboratoire d'Immunologie Moléculaire, Département de Microbiologie et Immunologie, Université de Montréal, QC, Canada.
Mathieu HoudeInstitut de recherche en immunologie et en cancérologie, IRIC, Université de Montréal, QC, Canada.
Martin BarilInstitut de recherche en immunologie et en cancérologie, IRIC, Université de Montréal, QC, Canada.
Klaus FrühVaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, OR, USA.
Abdelaziz AmraniDépartement de Pédiatrie, Service d'Immunologie et d'Allergologie, Université de Sherbrooke, Sherbrooke, QC, Canada.
Satoshi IshidoLaboratory of Infectious Immunity, Yokohama Institute, Research Center for Allergy and Immunology, Japan.
Daniel LamarreInstitut de recherche en immunologie et en cancérologie, IRIC, Université de Montréal, QC, Canada.
Jacques ThibodeauLaboratoire d'Immunologie Moléculaire, Département de Microbiologie et Immunologie, Université de Montréal, QC, Canada.
Université de Montréal · CAChildren's Cancer Therapy Development Institute · USInstitute for Research in Immunology and Cancer · CARIKEN Center for Integrative Medical Sciences · JPUniversité de Sherbrooke · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to their classical antigen presenting functions, MHC class II molecules potentiate the TLR-triggered production of pro-inflammatory cytokines. Here, we have addressed the effect of Tollip and MARCH1 on the regulation of MHC II trafficking and TLR signaling. Our results show that MARCH1-deficient mice splenocytes are impaired in their capacity to produce pro-inflammatory cytokines in response to poly(I:C) and that TLR3 and MHC II molecules interact in the endocytic pathway. Knocking down Tollip expression in human CIITA(+) HeLa cells increased expression of HLA-DR but reduced the proportion of MHC II molecules associated with the CLIP peptide. Truncation of the HLA-DR cytoplasmic tails abrogated the effect of Tollip on MHC class II expression. While overexpression of Tollip did not affect HLA-DR levels, it antagonized the function of co-transfected MARCH1. We found that Tollip strongly reduced MARCH1 protein levels and that the two molecules appear to compete for binding to MHC II molecules. Altogether, our results demonstrate that Tollip regulates MHC class II trafficking and that MARCH1 may represent a new Tollip target.

Indexed as

Antigen presentationAPCs, antigen presenting cellsBtk, Bruton tyrosine kinaseC2, internal protein kinase C conserved region 2CIITA, class II trans-activatorCUE, coupling of ubiquitin to endoplasmic reticulum degradation domainDCs, dendritic cellsiDCs, immature DCsIL-1RAcP, IL-1R-associated proteinIL-1RI, IL-1 receptorIRAK, IL-1 receptor-associated kinaseMARCH1MARCH, membrane-associated RING-CHMFVs, mean fluorescence valuesMHC IIMHC II, MHC class IIMIR, modulator of immune recognitionPAMPs, pathogen-associated molecular patternsSOCS1, suppressor of cytokine signaling 1TBD, Tom1-binding domainTfr, transferrin receptorTGFBR1, TGF-beta type I receptorTIR, Toll/IL-1 receptorTLR3TLR, toll-like receptorTollipTollip, Toll-interacting protein

Identifiers

PMID24600555
PMCPMC3908327
OpenAlexW1997977228

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.