Evidence map›Paper›PMID 17620357›Full record

ArticleInfection and immunity2007

Slc11a1, formerly Nramp1, is expressed in dendritic cells and influences major histocompatibility complex class II expression and antigen-presenting cell function.

Carmel B Stober, Sven Brode, Jacqueline K White, Jean-François Popoff, Jenefer M Blackwell

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  13. Solute carrier protein family 11 member 1 (Slc11a1) activation efficiently inhibitsJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2017
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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

5 authors at 2 institutions in 1 country.

Carmel B StoberCambridge Institute for Medical Research and Department of Medicine, Wellcome Trust/MRC Building, University of Cambridge School of Clinical Medicine, Addenbrookes Hospital, Hills Road, Cambridge CB2 2XY, United Kingdom.
Sven Brode
Jacqueline K White
Jean-François Popoff
Jenefer M Blackwell
University of Cambridge · GBAddenbrooke's Hospital · GB

Funding

Collaborative Development of a Vaccine against Cutaneous and Visceral LeishmaniasR01AI067874 · NIAID · UNIVERSITY OF IOWA · PI WILSON, MARY E · 2006 to 2010
$2.2M
NIAID NIH HHS R01 AI067874Wellcome Trust 065642
6 · The paper itself

Abstract

Solute carrier family 11 member a1 (Slc11a1; formerly Nramp1) encodes a late endosomal/lysosomal protein/divalent cation transporter that regulates iron homeostasis in macrophages. During macrophage activation, Slc11a1 has multiple pleiotropic effects on gene regulation and function, including gamma interferon-induced class II expression and antigen-presenting cell function. The wild-type allele at Slc11a1 has been associated with a bias in Th1 cell function in vivo, which is beneficial in resistance to infection against intracellular macrophage pathogens but detrimental in contributing to development of type 1 diabetes. The extent to which this depends on macrophage versus dendritic cell (DC) function is not known. Here we show that Slc11a1 is expressed in late endosomes and/or lysosomes of CD11c(+) DCs. DCs from mutant and congenic wild-type mice upregulate interleukin-12 (IL-12) and IL-10 mRNA in response to lipopolysaccharide (LPS) stimulation, but the ratio of IL-10 to IL-12 is higher in unstimulated DCs and DCs stimulated for 15 h with LPS from mutant mice than from wild-type mice. DCs from wild-type mice upregulate major histocompatibility complex class II in response to LPS more efficiently than DCs from mutant mice. Unstimulated DCs from wild-type and mutant mice present ovalbumin (OVA) peptide with an efficiency equivalent to that of an OVA-specific CD4 T-cell line, but DCs from wild-type mice are more efficient at processing and presenting OVA or Leishmania activator of cell kinase (LACK) protein to OVA- and LACK-specific T cells. These data indicate that wild-type Slc11a1 expressed in DCs may play a role both in determining resistance to infectious disease and in susceptibility to autoimmune disease such as type 1 diabetes.

Indexed as

Gene Expression RegulationAnimalsAntigen PresentationAntigens, ProtozoanBiasCation Transport ProteinsCells, CulturedDendritic CellsEndosomesFlow CytometryHistocompatibility Antigens Class IIInterleukin-10Interleukin-12LeishmaniaLipopolysaccharidesLysosomesAntigens, ProtozoanCation Transport ProteinsHistocompatibility Antigens Class IIInterleukin-10Interleukin-12LACK antigen, LeishmaniaLipopolysaccharidesNatural Resistance-associated Macrophage Protein 1OvalbuminProtozoan ProteinsRNA, Messenger

Identifiers

PMID17620357
PMCPMC2044529
OpenAlexW2146904676

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.