Evidence map›Paper›PMID 36719379›Full record

ArticleThe Journal of clinical investigation2023

NLRP12 is an innate immune checkpoint for repressing IFN signatures and attenuating lupus nephritis progression.

Yen-Po Tsao, Fang-Yu Tseng, Chih-Wei Chao, Ming-Han Chen, Yi-Chen Yeh, Babamale Olarewaju Abdulkareem, Se-Yi Chen, Wen-Ting Chuang, Pei-Ching Chang, I-Chun Chen and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.5field-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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  8. Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Yen-Po TsaoInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
Fang-Yu TsengProgram in Molecular Medicine, National Yang Ming Chiao Tung University and Academia Sinica, Taipei, Taiwan.
Chih-Wei ChaoInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
Ming-Han ChenDivision of Allergy, Immunology and Rheumatology, Department of Medicine, and.
Yi-Chen YehDepartment of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Babamale Olarewaju AbdulkareemTaiwan International Graduate Program in Molecular Medicine, National Yang Ming Chiao Tung University and Academia Sinica, Taipei, Taiwan.
Se-Yi ChenDepartment of Neurosurgery, and.
Wen-Ting ChuangInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
Pei-Ching ChangInstitute of Microbiology and Immunology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
I-Chun ChenInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
Pin-Hsuan WangInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
Chien-Sheng WuDepartment of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
Chang-Youh TsaiDivision of Allergy, Immunology and Rheumatology, Department of Medicine, and.
Szu-Ting ChenInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
National Yang Ming Chiao Tung University · TWENT and Allergy · USFar Eastern Memorial Hospital · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signaling driven by nucleic acid sensors participates in interferonopathy-mediated autoimmune diseases. NLRP12, a pyrin-containing NLR protein, is a negative regulator of innate immune activation and type I interferon (IFN-I) production. Peripheral blood mononuclear cells (PBMCs) derived from systemic lupus erythematosus (SLE) patients expressed lower levels of NLRP12, with an inverse correlation with IFNA expression and high disease activity. NLRP12 expression was transcriptionally suppressed by runt-related transcription factor 1-dependent (RUNX1-dependent) epigenetic regulation under IFN-I treatment, which enhanced a negative feedback loop between low NLRP12 expression and IFN-I production. Reduced NLRP12 protein levels in SLE monocytes was linked to spontaneous activation of innate immune signaling and hyperresponsiveness to nucleic acid stimulations. Pristane-treated Nlrp12-/- mice exhibited augmented inflammation and immune responses; and substantial lymphoid hypertrophy was characterized in NLRP12-deficient lupus-prone mice. NLRP12 deficiency mediated the increase of autoantibody production, intensive glomerular IgG deposition, monocyte recruitment, and the deterioration of kidney function. These were bound in an IFN-I signature-dependent manner in the mouse models. Collectively, we reveal a remarkable link between low NLRP12 expression and lupus progression, which suggests the impact of NLRP12 on homeostasis and immune resilience.

Indexed as

Lupus Erythematosus, SystemicLupus NephritisNucleic AcidsAnimalsEpigenesis, GeneticImmunity, InnateInterferonsIntracellular Signaling Peptides and ProteinsLeukocytes, MononuclearMiceInterferonsIntracellular Signaling Peptides and ProteinsNLRP12 protein, mouseNucleic AcidsAutoimmunityCytokinesInflammationInnate immunityLupus

Identifiers

PMID36719379
PMCPMC9888378
OpenAlexW4318669135

What OpenQuestion holds

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LicenceCC BY
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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.