Evidence map›Paper›PMID 27377589›Full record

ArticleThe Journal of experimental medicine2016

Siglec-H protects from virus-triggered severe systemic autoimmunity.

Heike Schmitt, Sabrina Sell, Julia Koch, Martina Seefried, Sophia Sonnewald, Christoph Daniel, Thomas H Winkler, Lars Nitschke

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. The role of DAP12 in immune-related inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  10. Type I Interferon Production of Plasmacytoid Dendritic Cells under Control.International journal of molecular sciences · 2021
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Heike SchmittDivision of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.
Sabrina SellNikolaus-Fiebiger-Zentrum, Division of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.ORCID 0000-0002-4584-2733
Julia KochDivision of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.
Martina SeefriedNikolaus-Fiebiger-Zentrum, Division of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.ORCID 0000-0002-9870-3534
Sophia SonnewaldDivision of Biochemistry, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.ORCID 0000-0002-9185-6255
Christoph DanielDepartment of Nephropathology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.ORCID 0000-0002-6803-4755
Thomas H WinklerNikolaus-Fiebiger-Zentrum, Division of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany lars.nitschke@fau.de thomas.winkler@fau.de.
Lars NitschkeDivision of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany lars.nitschke@fau.de thomas.winkler@fau.de.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is controversial whether virus infections can contribute to the development of autoimmune diseases. Type I interferons (IFNs) are critical antiviral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus. Type I IFN is mainly produced by plasmacytoid dendritic cells (pDCs). The secretion of type I IFN of pDCs is modulated by Siglec-H, a DAP12-associated receptor on pDCs. In this study, we show that Siglec-H-deficient pDCs produce more of the type I IFN, IFN-α, in vitro and that Siglec-H knockout (KO) mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo. This did not impact control of viral replication. Remarkably, several weeks after a single mCMV infection, Siglec-H KO mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis. In contrast, uninfected aging Siglec-H KO mice developed a mild form of systemic autoimmunity. The induction of systemic autoimmune disease after virus infection in Siglec-H KO mice was accompanied by a type I IFN signature and fully dependent on type I IFN signaling. These results show that Siglec-H normally serves as a modulator of type I IFN responses after infection with a persistent virus and thereby prevents induction of autoimmune disease.

Indexed as

AnimalsDendritic CellsHerpesviridae InfectionsInterferon-alphaLectinsLupus Erythematosus, SystemicMiceMice, KnockoutMuromegalovirusReceptors, Cell SurfaceInterferon-alphaLectinsReceptors, Cell SurfaceSiglech protein, mouse

Identifiers

PMID27377589
PMCPMC4986536
OpenAlexW2461317495

What OpenQuestion holds

Textmetadata
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.