Evidence map›Paper›PMID 40524344›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2026

Loss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.

Gantsetseg Tumurkhuu, Graziela Perri, Richard Moore, Lihong Huo, Arati Naveen Kumar, Richard Ainsworth, Trinitee Oliver, Gabriela De Los Santos, David Gibb, Jessica Carriere and 8 more

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. 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

18 authors.

Gantsetseg TumurkhuuCedars-Sinai Medical Center, Los Angeles, California.
Graziela PerriCedars-Sinai Medical Center, Los Angeles, California.
Richard MooreCedars-Sinai Medical Center, Los Angeles, California.
Lihong HuoCedars-Sinai Medical Center, Los Angeles, California.
Arati Naveen KumarCedars-Sinai Medical Center, Los Angeles, California.
Richard AinsworthCedars-Sinai Medical Center, Los Angeles, California.
Trinitee OliverCedars-Sinai Medical Center, Los Angeles, California.
Gabriela De Los SantosCedars-Sinai Medical Center, Los Angeles, California.
David GibbCedars-Sinai Medical Center, Los Angeles, California.
Jessica CarriereCedars-Sinai Medical Center, Los Angeles, California.
Jeong Min YuCedars-Sinai Medical Center, Los Angeles, California.ORCID https://orcid.org/0000-0002-9197-1878
Rachel AbuavCedars-Sinai Medical Center, Los Angeles, California.
Lindsy ForbessCedars-Sinai Medical Center, Los Angeles, California.
Daniel J WallaceCedars-Sinai Medical Center and University of California, Los Angeles.
Mariko IshimoriCedars-Sinai Medical Center and University of California, Los Angeles.
Wonwoo ShonCedars-Sinai Medical Center, Los Angeles, California.
Christian StehlikCedars-Sinai Medical Center, Los Angeles, California.
Caroline A JefferiesCedars-Sinai Medical Center, Los Angeles, California.ORCID https://orcid.org/0000-0002-8879-6722

Funding

A novel essential inflammasome component propagating inflammatory responsesR01AI134030 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI DORFLEUTNER, ANDREA, STEHLIK, CHRISTIAN · 2019 to 2023
$3.1M
TRIM21 as a regulator of UVB- and cytosolic DNA-driven IFN responses in lupusR56AR078279 · NIAMS · CEDARS-SINAI MEDICAL CENTER · PI JEFFERIES, CAROLINE · 2022 to 2022
$367k
Cedars-Sinai Leon Fine Translational Science AwardCenter for Research in Women's Health Science, Cedars-SinaiNIAID NIH HHS R01 AI134030NIAMS NIH HHS R56 AR078279NIH HHS 1R56AR078279-01A1NIH HHS R01AI134030NIH HHS R03HL15863
6 · The paper itself

Abstract

objectivePatients with systemic lupus erythematosus (SLE) experience photosensitivity, with exposure to UVB light driving lupus flares and triggering symptoms like joint pain, fatigue, and cutaneous lesions. Although the mechanism(s) linking UVB exposure to systemic effects are unclear, type I interferons (IFNs) are known to play a role. Our previous work has shown that TRIM21, an autoantigen in SLE, functions as a negative regulator on the pathways driving IFN expression. Here we explore how TRIM21 functions to regulate both local and systemic inflammation following UVB exposure and how altered expression may drive cutaneous inflammation and photosensitivity in SLE.

methodsWild-type (WT; C57BL/6) and Trim21

resultsInfiltration of inflammatory cells and induction of type I IFN developed in UVB-exposed areas in both sets of mice. Most notably after UVB exposure, we observed splenomegaly and enhanced expression of IFN-stimulated genes in the blood and spleen of Trim21

conclusionTaken together, our results indicate that TRIM21 protects against IFN induction at both local and systemic levels by restricting STING signaling.

Identifiers

PMID40524344
PMCPMC12326329

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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.