Evidence map›Paper›PMID 25180065›Full record

ArticleThe Journal of experimental medicine2014

Early, transient depletion of plasmacytoid dendritic cells ameliorates autoimmunity in a lupus model.

Sarah L Rowland, Jeffrey M Riggs, Susan Gilfillan, Mattia Bugatti, William Vermi, Roland Kolbeck, Emil R Unanue, Miguel A Sanjuan, Marco Colonna

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed
25.2field-weighted citation impact, top 1% 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

181 citing papers in PubMed, 269 citations in OpenAlex.

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  8. Frontiers in cellular neuroscience · 2026
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121 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Sarah L RowlandDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.
Jeffrey M RiggsRespiratory, Inflammation and Autoimmunity Research Department, MedImmune, Gaithersburg, MD 20878.
Susan GilfillanDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.
Mattia BugattiDepartment of Pathology, University of Brescia, 25123 Brescia, Italy.
William VermiDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 Department of Pathology, University of Brescia, 25123 Brescia, Italy.
Roland KolbeckRespiratory, Inflammation and Autoimmunity Research Department, MedImmune, Gaithersburg, MD 20878.
Emil R UnanueDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.
Miguel A SanjuanRespiratory, Inflammation and Autoimmunity Research Department, MedImmune, Gaithersburg, MD 20878.
Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 mcolonna@pathology.wustl.edu.
Washington University in St. Louis · USUniversity of Brescia · IT

Funding

TRAINING PROGRAM IN IMMUNOLOGY AND IMMUNOGENETICST32AI007163 · NIAID · WASHINGTON UNIVERSITY · PI Kenneth M Murphy, Kodi S Ravichandran · 1985 to 2026
$14.8M
NIAID NIH HHS 5T32AI007163-35NIAID NIH HHS T32 AI007163
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) have long been implicated in the pathogenesis of lupus. However, this conclusion has been largely based on a correlative link between the copious production of IFN-α/β by pDCs and the IFN-α/β "signature" often seen in human lupus patients. The specific contribution of pDCs to disease in vivo has not been investigated in detail. For this reason, we generated a strain of BXSB lupus-prone mice in which pDCs can be selectively depleted in vivo. Early, transient ablation of pDCs before disease initiation resulted in reduced splenomegaly and lymphadenopathy, impaired expansion and activation of T and B cells, reduced antibodies against nuclear autoantigens and improved kidney pathology. Amelioration of pathology coincided with decreased transcription of IFN-α/β-induced genes in tissues. PDC depletion had an immediate impact on the activation of immune cells, and importantly, the beneficial effects on pathology were sustained even though pDCs later recovered, indicating an early pDC contribution to disease. Together, our findings demonstrate a critical function for pDCs during the IFN-α/β-dependent initiation of autoimmune lupus and point to pDCs as an attractive therapeutic target for the treatment of SLE.

Indexed as

Disease Models, AnimalAnimalsAutoimmunityDendritic CellsEnzyme-Linked Immunosorbent AssayFlow CytometryGlomerulonephritisInterferon-alphaInterferon-betaLupus Erythematosus, SystemicMiceMice, Mutant StrainsReal-Time Polymerase Chain ReactionStatistics, NonparametricInterferon-alphaInterferon-beta

Identifiers

PMID25180065
PMCPMC4172228
OpenAlexW2053111002

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.