Evidence map›Paper›PMID 29052537›Full record

ArticleArthritis research & therapy2017

Enhanced IFN-α production is associated with increased TLR7 retention in the lysosomes of palasmacytoid dendritic cells in systemic lupus erythematosus.

Goh Murayama, Nanako Furusawa, Asako Chiba, Ken Yamaji, Naoto Tamura, Sachiko Miyake

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 70 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Goh MurayamaDepartment of Immunology, Juntendo University School of Medicine, 2-2-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Nanako FurusawaDepartment of Immunology, Juntendo University School of Medicine, 2-2-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Asako ChibaDepartment of Immunology, Juntendo University School of Medicine, 2-2-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. a-chiba@juntendo.ac.jp.
Ken YamajiDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Naoto TamuraDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Sachiko MiyakeDepartment of Immunology, Juntendo University School of Medicine, 2-2-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. s-miyake@juntendo.ac.jp.
Juntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterferon-α (IFN-α) is increased and plays an important role in the pathogenesis of systemic lupus erythematosus (SLE). Plasmacytoid dendritic cells (pDCs) are the main producer of IFN-α, but their IFN-α producing capacity has been shown to be unchanged or reduced when stimulated with a Toll-like receptor 9 (TLR9) agonist in patients with SLE compared to in healthy individuals. In this study, we investigated the IFN-α-producing capacity of lupus pDCs under different stimulation.

methodspDCs from patients with SLE and healthy controls (HC) were stimulated with TLR9 or TLR7 agonist, and their IFN-α producing capacity was examined by intracellular cytokine staining and flow cytometry. The correlation of IFN-α-producing capacity with serum IFN-α levels and disease activity was assessed. The effect of in vitro IFN-α exposure on IFN-α production by pDCs was examined. Localization of TLR7 in cellular compartments in pDCs was investigated.

resultsThe IFN-α producing capacity of pDCs was reduced after TLR9 stimulation, but increased when stimulated with a TLR7 agonist in SLE compared to in HC. IFN-α production by pDCs upon TLR9 stimulation was reduced and the percentage of IFN-α

conclusionsThese findings indicate that enhanced TLR7 responses of lupus pDCs, owing to TLR7 retention in late endosome/lysosome and exposure to IFN-α, are associated with the pathogenesis of SLE.

Indexed as

AdultDendritic CellsFemaleHumansInterferon-alphaLupus Erythematosus, SystemicLysosomesMaleMiddle AgedToll-Like Receptor 7Young AdultInterferon-alphaTLR7 protein, humanToll-Like Receptor 7Interferon-αPlasmacytoid dendritic cellsSystemic lupus erythematosusToll-like receptor

Identifiers

PMID29052537
PMCPMC5649081
OpenAlexW2766880350

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Registered trials

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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.