Evidence map›Paper›PMID 38478694›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

A type I interferon regulatory network for human plasmacytoid dendritic cells based on heparin, membrane-bound and soluble BDCA-2.

Francisco Venegas-Solis, Laura Staliunaite, Elisa Rudolph, Carina Chan-Song Münch, Philipp Yu, Sven-A Freibert, Takahiro Maeda, Christine L Zimmer, Christian Möbs, Christian Keller and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. 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

12 authors at 2 institutions in 2 countries.

Francisco Venegas-SolisInstitute for Immunology, Philipps-Universität Marburg, Biomedizinisches Forschungszentrum Marburg, Marburg 35043, Germany.ORCID 0000-0001-5799-8711
Laura StaliunaiteInstitute for Immunology, Philipps-Universität Marburg, Biomedizinisches Forschungszentrum Marburg, Marburg 35043, Germany.ORCID 0009-0005-5609-7643
Elisa RudolphInstitute for Immunology, Philipps-Universität Marburg, Biomedizinisches Forschungszentrum Marburg, Marburg 35043, Germany.
Carina Chan-Song MünchInstitute of Virology, Philipps-Universität Marburg, Biomedizinisches Forschungszemtrum Marburg, Marburg 35043, Germany.
Philipp YuInstitute for Immunology, Philipps-Universität Marburg, Biomedizinisches Forschungszentrum Marburg, Marburg 35043, Germany.
Sven-A FreibertInstitute for Cytobiology, Center for Synthetic Microbiology, Philipps-Universität Marburg, Marburg 35032, Germany.ORCID 0000-0002-8521-2963
Takahiro MaedaDepartment of Island and Community Medicine, Island Medical Research Institute, Nagasaki University Graduate School of Biomedical Science, Nagasaki 852-8523, Japan.ORCID 0009-0003-0217-0775
Christine L ZimmerDepartment of Dermatology and Allergology, Philipps-Universität Marburg, Marburg 35043, Germany.
Christian MöbsDepartment of Dermatology and Allergology, Philipps-Universität Marburg, Marburg 35043, Germany.ORCID 0000-0002-5197-7669
Christian KellerInstitute of Virology, Philipps-Universität Marburg, Biomedizinisches Forschungszemtrum Marburg, Marburg 35043, Germany.ORCID 0000-0002-0075-7199
Andreas KaufmannInstitute for Immunology, Philipps-Universität Marburg, Biomedizinisches Forschungszentrum Marburg, Marburg 35043, Germany.ORCID 0000-0002-3936-5379
Stefan BauerInstitute for Immunology, Philipps-Universität Marburg, Biomedizinisches Forschungszentrum Marburg, Marburg 35043, Germany.
Philipps University of Marburg · DENagasaki University · JP

Funding

Deutsche Forschungsgemeinschaft (DFG) 114933180-TR84Deutsche Forschungsgemeinschaft (DFG) 369799452 - TRR237
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) produce type I interferons (IFNs) after sensing viral/bacterial RNA or DNA by toll-like receptor (TLR) 7 or TLR9, respectively. However, aberrant pDCs activation can cause adverse effects on the host and contributes to the pathogenesis of type I IFN-related autoimmune diseases. Here, we show that heparin interacts with the human pDCs-specific blood dendritic cell antigen 2 (BDCA-2) but not with related lectins such as DCIR or dectin-2. Importantly, BDCA-2-heparin interaction depends on heparin sulfation and receptor glycosylation and results in inhibition of TLR9-driven type I IFN production in primary human pDCs and the pDC-like cell line CAL-1. This inhibition is mediated by unfractionated and low-molecular-weight heparin, as well as endogenous heparin from plasma, suggesting that the local blood environment controls the production of IFN-α in pDCs. Additionally, we identified an activation-dependent soluble form of BDCA-2 (solBDCA-2) in human plasma that functions as heparin antagonist and thereby increases TLR9-driven IFN-α production in pDCs. Of importance, solBDCA-2 levels in the serum were increased in patients with scrub typhus (an acute infectious disease caused by

Indexed as

Autoimmune DiseasesInterferon Type IDendritic CellsHeparinHumansToll-Like Receptor 9HeparinInterferon Type IToll-Like Receptor 9BDCA-2glycosaminoglycansheparinplasmacytoid dendritic cellstype I interferons

Identifiers

PMID38478694
PMCPMC10963015
OpenAlexW4392777151

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.