Evidence map›Paper›PMID 38321013›Full record

ArticleNature communications2024

Smith-specific regulatory T cells halt the progression of lupus nephritis.

Peter J Eggenhuizen, Rachel M Y Cheong, Cecilia Lo, Janet Chang, Boaz H Ng, Yi Tian Ting, Julie A Monk, Khai L Loh, Ashraf Broury, Elean S V Tay and 12 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

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  18. Regulatory T Cell-Based Adoptive Cell Therapy in Autoimmunity.International journal of molecular sciences · 2025
    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

22 authors.

Peter J Eggenhuizen *Centre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.ORCID 0000-0002-7102-3547
Rachel M Y Cheong *Centre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.ORCID 0009-0009-6977-1333
Cecilia LoCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Janet ChangCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Boaz H NgCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Yi Tian TingCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Julie A MonkCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Khai L LohCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.ORCID 0000-0002-2211-2404
Ashraf BrouryCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.ORCID 0009-0008-0729-5223
Elean S V TayCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Chanjuan ShenDepartment of Hematology, The Affiliated Zhuzhou Hospital of Xiangya Medical College, Central South University, Zhuzhou, China.
Yong ZhongCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Steven LimAlfred Research Alliance Flow Cytometry Core Facility, Melbourne, VIC, Australia.ORCID 0000-0003-3663-0736
Jia Xi ChungCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Rangi Kandane-RathnayakeCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Rachel KoelmeyerCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Alberta HoiCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Ashutosh ChaudhryFormer Employee of Amgen, South San Francisco, CA, USA.
Paolo ManzanilloAmgen Research, Amgen Inc, South San Francisco, CA, USA.
Sarah L SnelgroveCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.ORCID 0009-0001-0031-6414
Eric F MorandCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.ORCID 0000-0002-9507-3338
Joshua D OoiCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia. Joshua.Ooi@monash.edu.ORCID 0000-0003-3328-2561

Funding

Amgen (Amgen Inc.) 100002429, 2021026213-001Department of Health | National Health and Medical Research Council (NHMRC) 501100000925, 2017877Lupus Research Alliance (Lupus Research Alliance, Inc.) 100012051, 588087 and 850279U.S. Department of Defense (United States Department of Defense) 100000005, LR210065
6 · The paper itself

Abstract

Antigen-specific regulatory T cells (Tregs) suppress pathogenic autoreactivity and are potential therapeutic candidates for autoimmune diseases such as systemic lupus erythematosus (SLE). Lupus nephritis is associated with autoreactivity to the Smith (Sm) autoantigen and the human leucocyte antigen (HLA)-DR15 haplotype; hence, we investigated the potential of Sm-specific Tregs (Sm-Tregs) to suppress disease. Here we identify a HLA-DR15 restricted immunodominant Sm T cell epitope using biophysical affinity binding assays, then identify high-affinity Sm-specific T cell receptors (TCRs) using high-throughput single-cell sequencing. Using lentiviral vectors, we transduce our lead Sm-specific TCR into Tregs derived from patients with SLE who are anti-Sm and HLA-DR15 positive. Compared with polyclonal mock-transduced Tregs, Sm-Tregs potently suppress Sm-specific pro-inflammatory responses in vitro and suppress disease progression in a humanized mouse model of lupus nephritis. These results show that Sm-Tregs are a promising therapy for SLE.

Indexed as

Lupus Erythematosus, SystemicLupus NephritisAnimalsAutoantigensHumansMiceT-Lymphocytes, RegulatoryAutoantigens

Identifiers

PMID38321013
PMCPMC10847119

What OpenQuestion holds

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LicenceCC BY
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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.