Evidence map›Paper›PMID 41029739›Full record

ArticleMobile DNA2025

Type I interferons increase expression of endogenous retrovirus K102 and envelope protein in myeloid cells from patients with autoimmune disease.

Ethan Le, Fatemeh Moadab, Xiaoxing Wang, Rayan Najjar, Alison Bays, Kathryn M Hastie, Jeremy Shek, Erica Ollmann Saphire, Tomas Mustelin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mobile DNA, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Ethan LeDivision of Rheumatology, Department of Medicine, University of Washington, 750 Republican Street, Room E507, Seattle, WA, 98109, USA.
Fatemeh MoadabDivision of Rheumatology, Department of Medicine, University of Washington, 750 Republican Street, Room E507, Seattle, WA, 98109, USA.
Xiaoxing WangDivision of Rheumatology, Department of Medicine, University of Washington, 750 Republican Street, Room E507, Seattle, WA, 98109, USA.
Rayan NajjarDivision of Rheumatology, Department of Medicine, University of Washington, 750 Republican Street, Room E507, Seattle, WA, 98109, USA.
Alison BaysDivision of Rheumatology, Department of Medicine, University of Washington, 750 Republican Street, Room E507, Seattle, WA, 98109, USA.
Kathryn M HastieCenter for Vaccine Innovation, Institute for Immunology, La Jolla, CA, USA.
Jeremy ShekCenter for Vaccine Innovation, Institute for Immunology, La Jolla, CA, USA.
Erica Ollmann SaphireCenter for Vaccine Innovation, Institute for Immunology, La Jolla, CA, USA.
Tomas MustelinDivision of Rheumatology, Department of Medicine, University of Washington, 750 Republican Street, Room E507, Seattle, WA, 98109, USA. tomas2@uw.edu.

Funding

RESEARCH TRAINING IN RHEUMATOLOGYT32AR007108 · NIAMS · UNIVERSITY OF WASHINGTON · PI Shaun Jackson, Tomas M Mustelin · 1986 to 2026
$6.6M
Upstream drivers of type I interferons in lupusR01AI186337 · NIAID · UNIVERSITY OF WASHINGTON · PI Joanne Michelle Kahlenberg, John LaCava · 2024 to 2026
$2.3M
Role of the L1 retrotransposon in interferon-positive SLER01AR081654 · NIAMS · UNIVERSITY OF WASHINGTON · PI Tomas M Mustelin · 2023 to 2026
$2.1M
Role of protein citrullination in rheumatoid arthritisR01AR074939 · NIAMS · UNIVERSITY OF WASHINGTON · PI MUSTELIN, TOMAS M · 2020 to 2024
$1.9M
Using Bioinformatics Methodologies to Explore the Role of Short Interspersed Elements in the Pathogenesis of Idiopathic Inflammatory MyopathiesK08AR082939 · NIAMS · UNIVERSITY OF WASHINGTON · PI Rayan Najjar · 2024 to 2026
$494k
HERV-K immunity, a trigger of citrullination in rheumatoid arthritis?R21AR077266 · NIAMS · UNIVERSITY OF WASHINGTON · PI MUSTELIN, TOMAS M · 2021 to 2022
$425k
CSR NIH HHS R01 AR074939, R01 AR081654, R01 AI186337, R21 AR077266, T32 AR007108, K08 AR082939NIAID NIH HHS R01 AI186337NIAMS NIH HHS K08 AR082939NIAMS NIH HHS R01 AR074939NIAMS NIH HHS R01 AR081654NIAMS NIH HHS R21 AR077266NIAMS NIH HHS T32 AR007108
6 · The paper itself

Abstract

backgroundAutoantibodies against envelope (Env) protein encoded by human endogenous retrovirus group K (HERV-K) are prevalent in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), but it remains unclear which proviruses are responsible for this autoantigen. It also remains poorly understood how the transcription of HERV-K loci is regulated in cells that can produce Env.

resultsWe aligned our neutrophil RNA sequencing data to the new telomere-to-telomere reference genome and found uniquely mapping transcripts from HERV-K101, K102, K104, K108, K109, K117 and ERVK5, of which only K102, K108, and K109 encode an intact Env. Expression of K102 and K108 were higher in SLE than in healthy donors or RA (p

conclusionsOur data establish a role for interferons in maintaining increased HERV-K expression in SLE and suggest that interferons or other cytokines can upregulate HERV-K to similar levels in RA. A transient increase may also accompany normal immune responses, suggesting that endogenous retroviruses may have been co-opted for efficient immune responses.

Indexed as

Endogenous retrovirus KEnvelopeInterferonLupusRheumatoid arthritisTNFα

Identifiers

PMID41029739
PMCPMC12486725

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.